404 results on '"Wiesner, Rudolf J."'
Search Results
2. Immortalised murine R349P desmin knock-in myotubes exhibit a reduced proton leak and decreased ADP/ATP translocase levels in purified mitochondria
- Author
-
Berwanger, Carolin, Terres, Dominic, Pesta, Dominik, Eggers, Britta, Marcus, Katrin, Wittig, Ilka, Wiesner, Rudolf J., Schröder, Rolf, and Clemen, Christoph S.
- Published
- 2024
- Full Text
- View/download PDF
3. Mitochondrial membrane proteins and VPS35 orchestrate selective removal of mtDNA
- Author
-
Sen, Ayesha, Kallabis, Sebastian, Gaedke, Felix, Jüngst, Christian, Boix, Julia, Nüchel, Julian, Maliphol, Kanjanamas, Hofmann, Julia, Schauss, Astrid C., Krüger, Marcus, Wiesner, Rudolf J., and Pla-Martín, David
- Published
- 2022
- Full Text
- View/download PDF
4. Preserved striatal innervation maintains motor function despite severe loss of nigral dopaminergic neurons.
- Author
-
Paß, Thomas, Ricke, Konrad M, Hofmann, Pierre, Chowdhury, Roy S, Nie, Yu, Chinnery, Patrick, Endepols, Heike, Neumaier, Bernd, Carvalho, André, Rigoux, Lionel, Steculorum, Sophie M, Prudent, Julien, Riemer, Trine, Aswendt, Markus, Liss, Birgit, Brachvogel, Bent, and Wiesner, Rudolf J
- Subjects
DOPAMINERGIC neurons ,MITOCHONDRIAL DNA ,SUBSTANTIA nigra ,PARKINSON'S disease ,INNERVATION - Abstract
Degeneration of dopaminergic neurons in the substantia nigra and their striatal axon terminals causes cardinal motor symptoms of Parkinson's disease. In idiopathic cases, high levels of mitochondrial DNA alterations, leading to mitochondrial dysfunction, are a central feature of these vulnerable neurons. Here we present a mouse model expressing the K320E variant of the mitochondrial helicase Twinkle in dopaminergic neurons, leading to accelerated mitochondrial DNA mutations. These K320E-Twinkle
DaN mice showed normal motor function at 20 months of age, although ∼70% of nigral dopaminergic neurons had perished. Remaining neurons still preserved ∼75% of axon terminals in the dorsal striatum and enabled normal dopamine release. Transcriptome analysis and viral tracing confirmed compensatory axonal sprouting of the surviving neurons. We conclude that a small population of substantia nigra dopaminergic neurons is able to adapt to the accumulation of mitochondrial DNA mutations and maintain motor control. [ABSTRACT FROM AUTHOR]- Published
- 2024
- Full Text
- View/download PDF
5. A keratin scaffold regulates epidermal barrier formation, mitochondrial lipid composition, and activity
- Author
-
Kumar, Vinod, Bouameur, Jamal-Eddine, Bär, Janina, Rice, Robert H, Hornig-Do, Hue-Tran, Roop, Dennis R, Schwarz, Nicole, Brodesser, Susanne, Thiering, Sören, Leube, Rudolf E, Wiesner, Rudolf J, Vijayaraj, Preethi, Brazel, Christina B, Heller, Sandra, Binder, Hans, Löffler-Wirth, Henry, Seibel, Peter, and Magin, Thomas M
- Subjects
Biochemistry and Cell Biology ,Biomedical and Clinical Sciences ,Biological Sciences ,Aetiology ,2.1 Biological and endogenous factors ,Animals ,Cell Adhesion ,Cell Membrane ,Cornified Envelope Proline-Rich Proteins ,DNA-Binding Proteins ,Epidermis ,Female ,Gene Expression Regulation ,Developmental ,Genotype ,Intermediate Filaments ,Keratinocytes ,Keratins ,Lipids ,Male ,Membrane Proteins ,Mice ,Mice ,Inbred C57BL ,Mice ,Knockout ,Mitochondria ,Proteome ,Transcription Factors ,Medical and Health Sciences ,Developmental Biology ,Biological sciences ,Biomedical and clinical sciences - Abstract
Keratin intermediate filaments (KIFs) protect the epidermis against mechanical force, support strong adhesion, help barrier formation, and regulate growth. The mechanisms by which type I and II keratins contribute to these functions remain incompletely understood. Here, we report that mice lacking all type I or type II keratins display severe barrier defects and fragile skin, leading to perinatal mortality with full penetrance. Comparative proteomics of cornified envelopes (CEs) from prenatal KtyI(-/-) and KtyII(-/-)(K8) mice demonstrates that absence of KIF causes dysregulation of many CE constituents, including downregulation of desmoglein 1. Despite persistence of loricrin expression and upregulation of many Nrf2 targets, including CE components Sprr2d and Sprr2h, extensive barrier defects persist, identifying keratins as essential CE scaffolds. Furthermore, we show that KIFs control mitochondrial lipid composition and activity in a cell-intrinsic manner. Therefore, our study explains the complexity of keratinopathies accompanied by barrier disorders by linking keratin scaffolds to mitochondria, adhesion, and CE formation.
- Published
- 2015
6. The Impact of Mitochondrial Dysfunction on Dopaminergic Neurons in the Olfactory Bulb and Odor Detection
- Author
-
Paß, Thomas, Aßfalg, Marlene, Tolve, Marianna, Blaess, Sandra, Rothermel, Markus, Wiesner, Rudolf J., and Ricke, Konrad M.
- Published
- 2020
- Full Text
- View/download PDF
7. Immortalised murine R349P desmin knock-in myotubes exhibit a reduced proton leak and decreased ADP/ATP translocase levels in purified mitochondria
- Author
-
Berwanger, Carolin, primary, Terres, Dominic, additional, Pesta, Dominik, additional, Eggers, Britta, additional, Marcus, Katrin, additional, Wittig, Ilka, additional, Wiesner, Rudolf J, additional, Schroeder, Rolf, additional, and Clemen, Christoph Stephan, additional
- Published
- 2023
- Full Text
- View/download PDF
8. Imbalance of Mitochondrial Respiratory Chain Complexes in the Epidermis Induces Severe Skin Inflammation
- Author
-
Weiland, Daniela, Brachvogel, Bent, Hornig-Do, Hue-Tran, Neuhaus, Johannes F.G., Holzer, Tatjana, Tobin, Desmond J., Niessen, Carien M., Wiesner, Rudolf J., and Baris, Olivier R.
- Published
- 2018
- Full Text
- View/download PDF
9. Epithelial loss of mitochondrial oxidative phosphorylation leads to disturbed enamel and impaired dentin matrix formation in postnatal developed mouse incisor
- Author
-
Imhof, Thomas, Rosenblatt, Katharina, Pryymachuk, Galyna, Weiland, Daniela, Noetzel, Nicolas, Deschner, James, Baris, Olivier R., Kimoloi, Sammy, Koch, Manuel, Wiesner, Rudolf J., and Korkmaz, Yüksel
- Published
- 2020
- Full Text
- View/download PDF
10. Metformin causes a futile intestinal–hepatic cycle which increases energy expenditure and slows down development of a type 2 diabetes-like state
- Author
-
Schommers, Philipp, Thurau, Anna, Bultmann-Mellin, Insa, Guschlbauer, Maria, Klatt, Andreas R., Rozman, Jan, Klingenspor, Martin, de Angelis, Martin Hrabe, Alber, Jens, Gründemann, Dirk, Sterner-Kock, Anja, and Wiesner, Rudolf J.
- Published
- 2017
- Full Text
- View/download PDF
11. Mosaic Deficiency in Mitochondrial Oxidative Metabolism Promotes Cardiac Arrhythmia during Aging
- Author
-
Baris, Olivier R., Ederer, Stefan, Neuhaus, Johannes F.G., von Kleist-Retzow, Jürgen-Christoph, Wunderlich, Claudia M., Pal, Martin, Wunderlich, F. Thomas, Peeva, Viktoriya, Zsurka, Gabor, Kunz, Wolfram S., Hickethier, Tilman, Bunck, Alexander C., Stöckigt, Florian, Schrickel, Jan W., and Wiesner, Rudolf J.
- Published
- 2015
- Full Text
- View/download PDF
12. CLPP coordinates mitoribosomal assembly through the regulation of ERAL1 levels
- Author
-
Szczepanowska, Karolina, Maiti, Priyanka, Kukat, Alexandra, Hofsetz, Eduard, Nolte, Hendrik, Senft, Katharina, Becker, Christina, Ruzzenente, Benedetta, Hornig‐Do, Hue‐Tran, Wibom, Rolf, Wiesner, Rudolf J, Krüger, Marcus, and Trifunovic, Aleksandra
- Published
- 2016
- Full Text
- View/download PDF
13. Combined fibre atrophy and decreased muscle regeneration capacity driven by mitochondrial DNA alterations underlie the development of sarcopenia
- Author
-
Kimoloi, Sammy, primary, Sen, Ayesha, additional, Guenther, Stefan, additional, Braun, Thomas, additional, Brügmann, Tobias, additional, Sasse, Philipp, additional, Wiesner, Rudolf J., additional, Pla‐Martín, David, additional, and Baris, Olivier R., additional
- Published
- 2022
- Full Text
- View/download PDF
14. Mitochondrial respiration in B lymphocytes is essential for humoral immunity by controlling the flux of the TCA cycle
- Author
-
Urbanczyk, Sophia, primary, Baris, Olivier R., additional, Hofmann, Jörg, additional, Taudte, R. Verena, additional, Guegen, Naïg, additional, Golombek, Florian, additional, Castiglione, Kathrin, additional, Meng, Xianyi, additional, Bozec, Aline, additional, Thomas, Jana, additional, Weckwerth, Leonie, additional, Mougiakakos, Dimitrios, additional, Schulz, Sebastian R., additional, Schuh, Wolfgang, additional, Schlötzer-Schrehardt, Ursula, additional, Steinmetz, Tobit D., additional, Brodesser, Susanne, additional, Wiesner, Rudolf J., additional, and Mielenz, Dirk, additional
- Published
- 2022
- Full Text
- View/download PDF
15. Novel Pathogenic Sequence Variation m.5789T > C Causes NARP Syndrome and Promotes Formation of Deletions of the Mitochondrial Genome
- Author
-
Hippen, Marius, Zsurka, Gabor, Peeva, Viktoriya, Machts, Judith, Schwiecker, Kati, Debska-Vielhaber, Grazyna, Wiesner, Rudolf J., Vielhaber, Stefan, Kunz, Wolfram S., Hippen, Marius, Zsurka, Gabor, Peeva, Viktoriya, Machts, Judith, Schwiecker, Kati, Debska-Vielhaber, Grazyna, Wiesner, Rudolf J., Vielhaber, Stefan, and Kunz, Wolfram S.
- Abstract
Background and Objectives We report the pathogenic sequence variant m.5789T>C in the anticodon stem of the mitochondrial tRNA for cysteine as a novel cause of neuropathy, ataxia, and retinitis pigmentosa (NARP), which is usually associated with pathogenic variants in the MT-ATP6 gene. Methods To address the correlation of oxidative phosphorylation deficiency with mutation loads, we performed genotyping on single laser-dissected skeletal muscle fibers. Stability of the mitochondrial tRNA(Cys) was investigated by Northern blotting. Accompanying deletions of the mitochondrial genome were detected by long-range PCR and their breakpoints were determined by sequencing of single-molecule amplicons. Results The sequence variant m.5789T>C, originating from the patient's mother, decreases the stability of the mitochondrial tRNA for cysteine by disrupting the anticodon stem, which subsequently leads to a combined oxidative phosphorylation deficiency. In parallel, we observed a prominent cluster of low-abundance somatic deletions with breakpoints in the immediate vicinity of the m.5789T>C variant. Strikingly, all deletion-carrying mitochondrial DNA (mtDNA) species, in which the corresponding nucleotide position was not removed, harbored the mutant allele, and none carried the wild-type allele. Discussion In addition to providing evidence for the novel association of a tRNA sequence alteration with NARP syndrome, our observations support the hypothesis that single nucleotide changes can lead to increased occurrence of site-specific mtDNA deletions through the formation of an imperfect repeat. This finding might be relevant for understanding mechanisms of deletion generation in the human mitochondrial genome.
- Published
- 2022
16. Combined fibre atrophy and decreased muscle regeneration capacity driven by mitochondrial DNA alterations underlie the development of sarcopenia
- Author
-
Kimoloi, Sammy, Sen, Ayesha, Guenther, Stefan, Braun, Thomas, Brugmann, Tobias, Sasse, Philipp, Wiesner, Rudolf J., Pla-Martin, David, Baris, Olivier R., Kimoloi, Sammy, Sen, Ayesha, Guenther, Stefan, Braun, Thomas, Brugmann, Tobias, Sasse, Philipp, Wiesner, Rudolf J., Pla-Martin, David, and Baris, Olivier R.
- Abstract
Background Mitochondrial dysfunction caused by mitochondrial (mtDNA) deletions have been associated with skeletal muscle atrophy and myofibre loss. However, whether such defects occurring in myofibres cause sarcopenia is unclear. Also, the contribution of mtDNA alterations in muscle stem cells (MuSCs) to sarcopenia remains to be investigated. Methods We expressed a dominant-negative variant of the mitochondrial helicase, which induces mtDNA alterations, specifically in differentiated myofibres (K320E(skm) mice) and MuSCs (K320E(msc) mice), respectively, and investigated their impact on muscle structure and function by immunohistochemistry, analysis of mtDNA and respiratory chain content, muscle transcriptome and functional tests. Results K320E(skm) mice at 24 months of age had higher levels of mtDNA deletions compared with controls in soleus (SOL, 0.07673% vs. 0.00015%, P = 0.0167), extensor digitorum longus (EDL, 0.0649 vs. 0.000925, P = 0.0015) and gastrocnemius (GAS, 0.09353 vs. 0.000425, P = 0.0004). K320E(skm) mice revealed a progressive increase in the proportion of cytochrome c oxidase deficient (COX-) fibres in skeletal muscle cross sections, reaching a maximum of 3.03%, 4.36%, 13.58%, and 17.08% in EDL, SOL, tibialis anterior (TA) and GAS, respectively. However, mice did not show accelerated loss of muscle mass, muscle strength or physical performance. Histological analyses revealed ragged red fibres but also stimulated regeneration, indicating activation of MuSCs. RNAseq demonstrated enhanced expression of genes associated with protein synthesis, but also degradation, as well as muscle fibre differentiation and cell proliferation. In contrast, 7 days after destruction by cardiotoxin, regenerating TA of K320E(msc) mice showed 30% of COX- fibres. Notably, regenerated muscle showed dystrophic changes, increased fibrosis (2.5% vs. 1.6%, P = 0.0003), increased abundance of fat cells (2.76% vs. 0.23%, P = 0.0144) and reduced muscle mass (regenerated TA: 40.0 mg
- Published
- 2022
17. Mitochondrial respiration in B lymphocytes is essential for humoral immunity by controlling the flux of the TCA cycle
- Author
-
Urbanczyk, Sophia, Baris, Olivier R., Hofmann, Joerg, Taudte, R. Verena, Guegen, Naig, Golombek, Florian, Castiglione, Kathrin, Meng, Xianyi, Bozec, Aline, Thomas, Jana, Weckwerth, Leonie, Mougiakakos, Dimitrios, Schulz, Sebastian R., Schuh, Wolfgang, Schloetzer-Schrehardt, Ursula, Steinmetz, Tobit D., Brodesser, Susanne, Wiesner, Rudolf J., Mielenz, Dirk, Urbanczyk, Sophia, Baris, Olivier R., Hofmann, Joerg, Taudte, R. Verena, Guegen, Naig, Golombek, Florian, Castiglione, Kathrin, Meng, Xianyi, Bozec, Aline, Thomas, Jana, Weckwerth, Leonie, Mougiakakos, Dimitrios, Schulz, Sebastian R., Schuh, Wolfgang, Schloetzer-Schrehardt, Ursula, Steinmetz, Tobit D., Brodesser, Susanne, Wiesner, Rudolf J., and Mielenz, Dirk
- Abstract
To elucidate the function of oxidative phosphorylation (OxPhos) during B cell differentiation, we employ CD23Cre-driven expression of the dominant-negative K320E mutant of the mitochondrial helicase Twinkle (DNT). DNT-expression depletes mitochondrial DNA during B cell maturation, reduces the abundance of respiratory chain protein subunits encoded by mitochondrial DNA, and, consequently, respiratory chain super complexes in activated B cells. Whereas B cell development in DNT mice is normal, B cell proliferation, germinal centers, class switch to IgG, plasma cell maturation, and T cell-dependent as well as T cell -independent humoral immunity are diminished. DNT expression dampens OxPhos but increases glycolysis in lipopolysaccharide and B cell receptor-activated cells. Lipopolysaccharide-activated DNT-B cells exhibit altered metabolites of glycolysis, the pentose phosphate pathway, and the tricarboxylic acid cycle and a lower amount of phosphatidic acid. Consequently, mTORC1 activity and BLIMP1 induction are curtailed, whereas HIF1a is stabilized. Hence, mitochondrial DNA controls the metabolism of activated B cells via OxPhos to foster humoral immunity.
- Published
- 2022
18. Inhibition of insulin/IGF‐1 receptor signaling protects from mitochondria‐mediated kidney failure
- Author
-
Ising, Christina, Koehler, Sybille, Brähler, Sebastian, Merkwirth, Carsten, Höhne, Martin, Baris, Olivier R, Hagmann, Henning, Kann, Martin, Fabretti, Francesca, Dafinger, Claudia, Bloch, Wilhelm, Schermer, Bernhard, Linkermann, Andreas, Brüning, Jens C, Kurschat, Christine E, Müller, Roman‐Ulrich, Wiesner, Rudolf J, Langer, Thomas, Benzing, Thomas, and Brinkkoetter, Paul Thomas
- Published
- 2015
- Full Text
- View/download PDF
19. Novel Pathogenic Sequence Variation m.5789T>C Causes NARP Syndrome and Promotes Formation of Deletions of the Mitochondrial Genome
- Author
-
Hippen, Marius, primary, Zsurka, Gábor, additional, Peeva, Viktoriya, additional, Machts, Judith, additional, Schwiecker, Kati, additional, Debska-Vielhaber, Grazyna, additional, Wiesner, Rudolf J., additional, Vielhaber, Stefan, additional, and Kunz, Wolfram S., additional
- Published
- 2022
- Full Text
- View/download PDF
20. Regulation of mitochondrial transcription by mitochondrial transcription factor A
- Author
-
Montoya, Julio, Perez-Martos, Acisclo, Garstka, Heike L., Wiesner, Rudolf J., Dhalla, Naranjan S., editor, Gellerich, Frank Norbert, editor, and Zierz, Stephan, editor
- Published
- 1997
- Full Text
- View/download PDF
21. Embelin inhibits endothelial mitochondrial respiration and impairs neoangiogenesis during tumor growth and wound healing
- Author
-
Coutelle, Oliver, Hornig‐Do, Hue‐Tran, Witt, Axel, Andree, Maria, Schiffmann, Lars M, Piekarek, Michael, Brinkmann, Kerstin, Seeger, Jens M, Liwschitz, Maxim, Miwa, Satomi, Hallek, Michael, Krönke, Martin, Trifunovic, Aleksandra, Eming, Sabine A, Wiesner, Rudolf J, Hacker, Ulrich T, and Kashkar, Hamid
- Published
- 2014
- Full Text
- View/download PDF
22. Mitochondrial physiology: Gnaiger Erich et al ― MitoEAGLE Task Group
- Author
-
Gnaiger, Erich, Aasander Frostner, Eleonor, Abdul Karim, Norwahidah, Abdel-Rahman, Engy Ali, Abumrad, Nada A, Acuna-Castroviejo, Dario, Adiele, Reginald C, Ahn, Bumsoo, Alencar, MB, Ali, Sameh S, Almeida, Angeles, Alton, Lesley, Alves, Marco G, Amati, Francesca, Amoedo, Nivea Dias, Amorim, Ricardo, Anderson, Ethan J, Andreadou, Ioanna, Antunes, Diana, Arago, Marc, Aral, Cenk, Arandarcikaite, Odeta, Arias-Reyes, Christian, Armand, Anne-Sophie, Arnould, Thierry, Avram, Vlad Florian, Axelrod, Christopher L, Bairam, Aida, Bailey, Damian M, Bajpeyi, Sudip, Bajzikova, Martina, Bakker, Barbara M, Barlow, Jonathan, Bardal, Tora, Banni, A, Bastos Sant'Anna Silva, Ana Carolina, Batterson, Philip, Battino, Maurizio, Bazil, Jason, Beard, Daniel A, Beleza, Jorge, Bednarczyk, Piotr, Bello, Fiona, Ben-Shachar, Dorit, Bento Guida, Jose Freitas, Bergdahl, Andreas, Berge, Rolf K, Bergmeister, Lisa, Bernardi, Paolo, Berridge, Michael V, Bettinazzi, Stefano, Bishop, David, Blier, Pierre U, Blindheim, Dan Filip, Boardman, Neoma T, Boetker, Hans Erik, Borchard, Sabine, Boros, Mihaly, Borsheim, Elisabet, Borras, Consuelo, Borutaite, Vilma, Botella, Javier, Bouillaud, Frederic, Bouitbir, Jamal, Boushel, Robert C, Bovard, Josh, Bravo-Sagua, Roberto, Breton, Sophie, Brown, David A, Brown, Guy C, Brown, Robert A, Brozinick, Joseph T, Buettner, Garry R, Burtscher, Johannes, Bustos, Matilde, Calabria, Elisa, Calbet, Jose A, Calzia, Enrico, Cannon, Daniel T, Cano Sanchez, Maria, Canto Alvarez, Carles, Cardinale, D, Cardoso, Luiza Helena Daltro, Carvalho, Eugenia, Casado Pinna, Marta, Cassar, Samantha, Castelo, Maria P, Castilho, Roger F, Cavalcanti-de-Albuquerque, Joao Paulo, Cecatto, Cristiane, Celen, Murat C, Cervinkova, Zuzana, Chabi, Beatrice, Chakrabarti, Lisa, Chakrabarti, Sasanka, Chaurasia, Bhagirath, Chen, Quan, Chicco, Adam J, Chinopoulos, Christos, Chowdhury, Subir K, Cizmarova, Beata, Clementi, Emilio, Coen, Paul M, Cohen, Bruce H, Coker, Robert H, Collin-Chenot, Anne, Coughlan, Melinda T, Coxito, Petro, Crisostomo, Luis, Crispim, Marcell, Crossland, Hannah, Dahdah, Norma, Dalgaard, Louise T, Dambrova, Maija, Danhelovska, Tereza, Darveau, Charles A, Darwin, Paula M, Das, Anibh M, Dash, Ranjan K, Davidova, Eliska, Davis, Michael S, Dayanidhi, Sudarshan, De Bem, Andreza Fabro, De Goede, Paul, De Palma, Clara, De Pinto, Vito, Dela, F, Dembinska-Kiec, Aldona, Detraux, Damien, Devaux, Yvan, Di Marcello, Marco, Di Paola, Floriana Jessica, Dias, Candida, Dias, Tania R, Diederich, Marc, Distefano, Giovanna, Djafarzadeh, Siamak, Doermann, Niklas, Doerrier, Carolina, Dong, Lan-Feng, Donnelly, Chris, Drahota, Zdenek, Duarte, Filipe Valente, Dubouchaud, Herve, Duchen, Michael R, Dumas, Jean-Francois, Durham, William J, Dymkowska, Dorota, Dyrstad, Sissel E, Dyson, Alex, Dzialowski, Edward M, Eaton, Simon, Ehinger, Johannes, Elmer, Eskil, Endlicher, Rene, Engin, Ayse B, Escames, Germaine, Evinova, Andrea, Ezrova, Zuzana, Falk, Marni Joy, Fell, David A, Ferdinandy, Peter, Ferko, Miroslav, Fernandez-Ortiz, Marisol, Erika, Fernandez-Vizarra, Ferreira, Julio Cesar Batista, Ferreira, Rita, Ferri, Alessandra, Festuccia, WT, Fessel, Joshua P, Filipovska, Aleksandra, Fisar, Zdenek, Fischer, Christine, Fischer, Michael, Fisher, Gordon, Fisher, Joshua J, Fontanesi, Flavia, Forbes-Hernandez, Tamara Y, Ford, Ellen, Fornaro, Mara, Fuertes Agudo, Marina, Fulton, Montana, Galina, Antonio, Galkin, Alexander, Gallee, Leon, Galli, Gina L, Gama Perez, Pau, Gan, Zhenji, Ganetzky, Rebecca, Gao, Yun, Garcia, Geovana S, Garcia-Rivas, Gerardo, Garcia-Roves, Pablo Miguel, Garcia-Souza, Luiz Felipe, Garlid, Keith D, Garrabou, Gloria, Garten, Antje, Gastaldelli, Amalia, Gayen, Jiaur, Genders, Amanda J, Genova, Maria Luisa, Giampieri, Francesca, Glatz, Jan FC, Giovarelli, Matteo, Goikoetxea Usandizaga, Naroa, Goncalo Teixeira da Silva, Rui, Goncalves, Debora Farina, Gonzalez-Armenta, Jenny L, Gonzalez-Francesqua, A, Gonzalez-Freire, Marta, Gonzalo, Hugo, Goodpaster, Bret H, Gorr, Thomas A, Gourlay, Campbell W, Grams, Bente, Granata, Cesare, Grefte, Sander, Grilo, Luis, Guarch, Meritxell Espino, Gueguen, Naig, Gumeni, Sentiljana, Haas, Clarissa B, Haavik, Jan, Hachmo, Yafit, Haendeler, Judith, Haider, Markus, Hajrulahovic, Anesa, Hamann, Andrea, Han, Jin, Han, Woo Hyun, Hancock, Chad R, Hand, Steven C, Handl, Jiri, Hansikova, Hana, Hardee, Justin P, Hargreaves, Ian P, Harper, Mary Ellen, Harrison, David K, Hassan, Hazirah, Hatakova, Zuzana, Hausenloy, Derek J, Heales, Simon JR, Heiestad, Christina, Hellgren, Kim T, Henrique, Alexandrino, Hepple, Russell T, Hernansanz-Agustin, Pablo, Hewakapuge, Sudinna, Hickey, Anthony J, Ho, Dieu Hien, Hoehn, Kyle L, Hoel, Frederik, Holland, Olivia J, Holloway, Graham P, Holzner, Lorenz, Hoppel, Charles L, Hoppeler, H, Hoppel, Florian, Houstek, Josef, Huete-Ortega, Maria, Hyrossova, Petra, Iglesias-Gonzalez, Javier, Indiveri, Cesare, Irving, Brian A, Isola, Raffaella, Iyer, Shilpa, Jackson, Christophe B, Jadiya, Pooja, Jana, Prado Fabian, Jandeleit-Dahm, K, Jang, David H, Jang, Young C, Janowska, Joanna, Jansen, Kirsten, Jansen-Duerr, Pidder, Jansone, Baiba, Jarmuszkiewicz, Wieslawa, Jaskiewicz, Anna, Jaspers, Richard T, Jedlicka, Jan, Jerome, Estaquier, Jespersen, Nichlas R, Jha, Rajan K, Joseph, Vincent, Juhasz, Laszlo, Jurczak, Michael J, Jurk, Diana, Kaambre, Tuuli, Kaczor, Jan J, Kainulainen, Heikki, Kampa, Rafal Pawel, Kandel, Sunil M, Kane, Daniel A, Kapferer, Werner, Kapnick, Senta, Kappler, Lisa, Karabatsiakis, Alexander, Karavaeva, Iuliia, Karkucinska-Wieckowska, Agnieszka, Kaur, Sarbjot, Keijer, Jaap, Keller, Markus A, Keppner, Gloria, Khamoui, Andy V, Kidere, Dita, Kilbaugh, Todd, Kim, Hyoung Kyu, Kim, Julian KS, Kimoloi, Sammy, Klepinin, Aleksandr, Klepinina, Lyudmila, Klingenspor, Martin, Klocker, Helmut, Komlódi, Timea, Kolasa, Iris, Koopman, Werner JH, Kopitar-Jerala, Natasa, Kowaltowski, Alicia J, Kozlov, Andrey V, Krajcova, Adela, Krako Jakovljevic, Nina, Kristal, Bruce S, Krycer, Jamer R, Kuang, Jujiao, Kucera, Otto, Kuka, Janis, Kwak, Hyo Bum, Kwast, Kurt, Kwon, Oh Sung, Laasmaa, Martin, Labieniec-Watala, Magdalena, Lai, Nicola, Lalic, Nebojsa M, Land, John M, Lane, Nick, Laner, Verena, Lanza, Ian R, Laouafa, Sofien, Larsen, Steen, Larsen, Terje S, Lavery, Gareth G, Lazou, Antigone, Ledo, Ana Margarida, Lee, Hong Kyu, Leeuwenburgh, Christiaan, Lehti, Maarit, Lemieux, Helene, Lenaz, Giorgio, Lerfall, Jorgen, Li, Pingan A, Li Puma, Lance, Liang, Liping, Liepins, Edgars, Lin, Chien-Te, Liu, Jiankang, Lopez, Luis C, Lucchinetti, Eliana, Ma, Tao, Macedo, Maria P, Machado, Ivo F, Maciej, Sarah, MacMillan-Crow, Lee Ann, Magalhaes, Jose, Magri, Andrea, Majtnerova, Pavlina, Makarova, Elina, Makrecka-Kuka, Marina, Malik, Afshan N, Marcouiller, Francois, Marechal, Amandine, Markova, Michaela, Markovic, Ivanka, Martin, Daniel S, Martins, Ana Dias, Martins, Joao D, Maseko, Tumisang Edward, Maull, Felicia, Mazat, Jean Pierre, McKenna, Helen T, McKenzie, Matthew, McMillan, Duncan GG, McStay, Gavin P, Menze, Michael A, Mendham, Amy, Mercer, John R, Merz, Tamara, Messina, Angela, Meszaros, Andras T, Methner, Axel, Michalak, Slawomir, Mila Guasch, Maria, Minuzzi, Luciele M, Misirkic Marjanovic, Maja, Moellering, Douglas R, Moisoi, Nicoleta, Molina, Anthony JA, Montaigne, David, Moore, Anthony L, Moore, Christy, Moreau, Kerrie, Moreira, Bruno P, Moreno-Sanchez, Rafael, Mracek, Tomas, Muccini, Anna Maria, Muntane, Jordi, Muntean, Danina M, Murray, Andrew J, Musiol, Eva, Nabben, Miranda, Nair, K Sreekumaran, Nehlin, Jan O, Nemec, Michal, Nesci, Salvatore, Neufer, P Darrell, Neuzil, Jiri, Neviere, Remi, Newsom, Sean A., Norman, Jennifer, Nozickova, Katerina, Nunes, Sara, Nuoffer, Jean-Marc, O'Brien, Kristin, O'Brien, Katie A, O'Gorman, Donal, Olgar, Yusuf, Oliveira, Ben, Oliveira, Jorge, Oliveira, Marcus F, Oliveira, Marcos Tulio, Oliveira, Pedro F, Oliveira, Paulo J, Olsen, Rolf Erik, Orynbayeva, Zulfiya, Osiewacz, Heinz D, Paez, Hector, Pak, Youngmi K, Pallotta, Maria L, Palmeira, Carlos M, Parajuli, Nirmala, Passos, Joao F, Passrugger, Manuela, Patel, Hemal H, Pavlova, Nadia, Pavlovic, Kasja, Pecina, Petr, Pedersen, Tina M, Perales, Jose Carlos, Pereira da Silva Grilo da Silva, Filomena, Pereira, Rita, Perez Valencia, Juan A, Perks, Kara L, Pesta, Dominik, Petit, Patrice X, Pettersen Nitschke, Ina Katrine, Pichaud, Nicolas, Pichler, Irene, Piel, Sarah, Pietka, Terri A, Pinho, Sonia A, Pino, Maria F, Pirkmajer, Sergej, Place, Nicolas, Plangger, Mario, Porter, Craig, Porter, Richard K, Preguica, Ines, Procaccio, Vincent, Prochownik, Edward V, Prola, Alexandre, Pulinilkunnil, Thomas, Puskarich, Michael A, Puurand, Marju, Radenkovic, Filip, Ramzan, Rabia, Rattan, Suresh IS, Reano, Simone, Reboredo, Patricia, Rees, Bernard B, Renner-Sattler, Kathrin, Rial, Eduardo, Robinson, Matthew M, Roden, Michael, Rodrigues, Ana Sofia, Rodriguez, Enrique, Rodriguez-Enriquez, Sara, Roesland, Gro Vatne, Rolo, Anabela Pinto, Ropelle, Eduardo R, Roshanravan, Baback, Rossignol, Rodrigue, Rossiter, Harry B, Rousar, Tomas, Rubelj, Ivica, Rybacka-Mossakowska, Joanna, Saada, Ann, Safaei, Zahra, Sarlak, Saharnaz, Salin, Karine, Salvadego, Desy, Sandi, Carmen, Saner, Nicholas, Santos, Diana, Sanz, Alberto, Sardao, Vilma, Sazanov, Leonid A, Scaife, Paula, Scatena, Roberto, Schartner, Melanie, Scheibye-Knudsen, Morten, Schilling, Jan M, Schlattner, Uwe, Schmitt, Sabine, Schneider Gasser, Edith Mariane, Schoenfeld, Peter, Schots, Pauke C, Schulz, Rainer, Schwarzer, Christoph, Scott, Graham R, Selman, Colin, Sendon, Pamella Marie, Shabalina, Irina G, Sharma, Pushpa, Sharma, Vipin, Shevchuk, Igor, Shirazi, Reza, Shiroma, Jonathan G, Siewiera, Karolina, Silber, Ariel M, Silva, Ana Maria, Sims, Carrie A, Singer, Dominique, Singh, Brijesh Kumar, Skolik, Robert A, Smenes, Benedikte Therese, Smith, James, Soares, Félix Alexandre Antunes, Sobotka, Ondrej, Sokolova, Inna, Solesio Torregrosa, M De la Encarnacion, Soliz, Jorge, Sonkar, Vijay K, Sova, Marina, Sowton, Alice P, Sparagna, Genevieve C, Sparks, Lauren M, Spinazzi, Marco, Stankova, Pavla, Starr, Jonathan, Stary, Creed, Stefan, Eduard, Stelfa, Gundega, Stepto, Nigel K, Stevanovic, Jelena, Stiban, Johnny, Stier, Antoine, Stocker, Roland, Storder, Julie, Sumbalova, Zuzana, Suomalainen, Wartiovaara Anu, Suravajhala, Prashanth, Svalbe, Baiba, Swerdlow, Russel H, Swiniuch, Daria, Szabo, Ildiko, Szewczyk, Adam, Szibor, Marten, Tanaka, Masashi, Tandler, Bernard, Tarnopolsky, Mark A, Tausan, Daniel, Tavernarakis, Nektarios, Tepp, Kersti, Teodoro, J, Thakkar, Himani, Thapa, Maheshwo, Thyfault, John P, Tomar, Dhanendra, Ton, Riccardo, Torp, May-Kristin, Torres-Quesada, Omar, Towheed, Atif, Treberg, Jason R, Tretter, Laszlo, Trewin, Adam J, Trifunovic, Aleksandra, Trivigno, Catherine, Tronstad, Karl Johan, Trougakos, Ioannis P, Truu, Laura, Tuncay, Erkan, Turan, Belma, Tyrrell, Daniel J, Urban, Tomas, Urner, Sofia, Valentine, Joseph Marco, Van Bergen, Nicole J, Van der Ende, Miranda, Varricchio, Frederick, Vaupel, Peter, Vella, Joanna, Vendelin, Marko, Verdaguer, IB, Vercesi, Anibal E, Vernerova, Andrea, Victor, Victor Manuel, Vieira Ligo Teixeira, Camila, Vidimce, Josif, Viel, Christian, Vieyra, Adalberto, Vilks, Karlis, Villena, Joseph A, Vincent, Vinnyfred, Vinogradov, Andrey D, Viscomi, Carlo, Vitorino, Rui Miguel Pinheiro, Vlachaki Walker, Julia, Vogt, Sebastian, Volani, Chiara, Volska, Kristine, Votion, Dominique-Marie, Vujacic-Mirski, Ksenija, Wagner, Brett A, Ward, Marie Louise, Warnsmann, Verena, Wasserman, David H, Watala, Cezary, Wei, Yau-Huei, Weinberger, Klaus M, White, Sarah, Whitfield, Jamie, Wickert, Anika, Wieckowski, Mariusz R, Wiesner, Rudolf J, Williams, Caroline M, Winwood-Smith, Hugh, Wohlgemuth, Stephanie E, Wohlwend, Martin, Wolff, Jonci Nikolai, Wrutniak-Cabello, Chantal, Wuest, Rob C I, Yokota, Takashi, Zablocki, Krzysztof, Zanon, Alessandra, Zanou, Nadege, Zaugg, Kathrin, Zaugg, Michael, Zdrazilova, Lucie, Zhang, Yong, Zhang, Yi Zhu, Zikova, Alena, Zischka, Hans, Zorzano, Antonio, Zujovic, Tijana, Zurmanova, Jitka, Zvejniece, Liga, Lagarrigue, Sylviane, Munro, Daniel, Pereira, Susana, Laranjinha, Joäo, Hecker, Matthias, Jusic, Amela, Prigione, Alessandro, Sommer, Natascha, Weissig, Volkmar, Guida, Bento, G, John G, Jones, JG, AMS - Tissue Function & Regeneration, AMS - Rehabilitation & Development, Physiology, Mito-Eagle - Evolution-Age-Gender-Lifestyle-Environment (Mito-Eagle), Oroboros Instruments, Dynamique Musculaire et Métabolisme (DMEM), Université de Montpellier (UM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), and Gnaiger Erich, Aasander Frostner Eleonor, Abdul Karim Norwahidah, Abdel-Rahman Engy Ali, Abumrad Nada A, Acuna-Castroviejo Dario, Adiele Reginald C, Ahn Bumsoo, Alencar Mayke Bezerra, Ali Sameh S, Almeida Angeles, Alton Lesley, Alves Marco G, Amati Francesca, Amoedo Nivea Dias, Amorim Ricardo, Anderson Ethan J, Andreadou Ioanna, Antunes Diana, Arago Marc, Aral Cenk, Arandarcikaite Odeta, Arias-Reyes Christian, Armand Anne-Sophie, Arnould Thierry, Avram Vlad F, Axelrod Christopher L, Bailey Damian M, Bairam Aida, Bajpeyi Sudip, Bajzikova Martina, Bakker Barbara M, Banni Aml, Bardal Tora, Barlow J, Bastos Sant'Anna Silva Ana Carolina, Batterson Philip M, Battino Maurizio, Bazil Jason N, Beard Daniel A, Bednarczyk Piotr, Beleza Jorge, Bello Fiona, Ben-Shachar Dorit, Bento Guida Jose Freitas, Bergdahl Andreas, Berge Rolf K, Bergmeister Lisa, Bernardi Paolo, Berridge Michael V, Bettinazzi Stefano, Bishop David J, Blier Pierre U, Blindheim Dan Filip, Boardman Neoma T, Boetker Hans Erik, Borchard Sabine, Boros Mihaly, Boersheim Elisabet, Borras Consuelo, Borutaite Vilma, Botella Javier, Bouillaud Frederic, Bouitbir Jamal, Boushel Robert C, Bovard Josh, Bravo-Sagua Roberto, Breton Sophie, Brown David A, Brown Guy C, Brown Robert Andrew, Brozinick Joseph T, Buettner Garry R, Burtscher Johannes, Bustos Matilde, Calabria Elisa, Calbet Jose AL, Calzia Enrico, Cannon Daniel T, Cano Sanchez Maria Consolacion, Canto Alvarez Carles, Cardinale Daniele A, Cardoso Luiza HD, Carvalho Eugenia, Casado Pinna Marta, Cassar Samantha, Castelo Rueda Maria Paulina, Castilho Roger F, Cavalcanti-de-Albuquerque Joao Paulo, Cecatto Cristiane, Celen Murat C, Cervinkova Zuzana, Chabi Beatrice, Chakrabarti Lisa, Chakrabarti Sasanka, Chaurasia Bhagirath, Chen Quan, Chicco Adam J, Chinopoulos Christos, Chowdhury Subir Kumar, Cizmarova Beata, Clementi Emilio, Coen Paul M, Cohen Bruce H, Coker Robert H, Collin-Chenot Anne, Coughlan Melinda T, Coxito Pedro, Crisostomo Luis, Crispim Marcell, Crossland Hannah, Dahdah Norma Ramon, Dalgaard Louise T, Dambrova Maija, Danhelovska Tereza, Darveau Charles-A, Darwin Paula M, Das Anibh Martin, Dash Ranjan K, Davidova Eliska, Davis Michael S, Dayanidhi Sudarshan, De Bem Andreza Fabro, De Goede Paul, De Palma Clara, De Pinto Vito, Dela Flemming, Dembinska-Kiec Aldona, Detraux Damian, Devaux Yvan, Di Marcello Marco, Di Paola Floriana Jessica, Dias Candida, Dias Tania R, Diederich Marc, Distefano Giovanna, Djafarzadeh Siamak, Doermann Niklas, Doerrier Carolina, Dong Lan-Feng, Donnelly Chris, Drahota Zdenek, Duarte Filipe Valente, Dubouchaud Herve, Duchen Michael R, Dumas Jean-Francois, Durham William J, Dymkowska Dorota, Dyrstad Sissel E, Dyson Alex, Dzialowski Edward M, Eaton Simon, Ehinger Johannes K, Elmer Eskil, Endlicher Rene, Engin Ayse Basak, Escames Germaine, Evinova Andrea, Ezrova Zuzana, Falk Marni J, Fell David A, Ferdinandy Peter, Ferko Miroslav, Fernandez-Ortiz Marisol, Fernandez-Vizarra Erika, Ferreira Julio Cesar B, Ferreira Rita Maria P, Ferri Alessandra, Fessel Joshua Patrick, Festuccia William T, Filipovska Aleksandra, Fisar Zdenek, Fischer Christine, Fischer Michael J, Fisher Gordon, Fisher Joshua J, Fontanesi Flavia, Forbes-Hernandez Tamara Y, Ford Ellen, Fornaro Mara, Fuertes Agudo Marina, Fulton Montana, Galina Antonio, Galkin Alexander, Gallee Leon, Galli Gina L J, Gama Perez Pau, Gan Zhenji, Ganetzky Rebecca, Gao Yun, Garcia Geovana S, Garcia-Rivas Gerardo, Garcia-Roves Pablo Miguel, Garcia-Souza Luiz F, Garlid Keith D, Garrabou Gloria, Garten Antje, Gastaldelli Amalia, Gayen Jiaur, Genders Amanda J, Genova Maria Luisa, Giampieri Francesca, Giovarelli Matteo, Glatz Jan FC, Goikoetxea Usandizaga Naroa, Goncalo Teixeira da Silva Rui, Goncalves Debora Farina, Gonzalez- Armenta Jenny L, Gonzalez-Franquesa Alba, Gonzalez-Freire Marta, Gonzalo Hugo, Goodpaster Bret H, Gorr Thomas A, Gourlay Campbell W, Grams Bente, Granata Cesare, Grefte Sander, Grilo Luis, Guarch Meritxell Espino, Gueguen Naig, Gumeni Sentiljana, Haas Clarissa, Haavik Jan, Hachmo Yafit, Haendeler Judith, Haider Markus, Hajrulahovic Anesa, Hamann Andrea, Han Jin, Han Woo Hyun, Hancock Chad R, Hand Steven C, Handl Jiri, Hansikova Hana, Hardee Justin P, Hargreaves Iain P, Harper Mary- Ellen, Harrison David K, Hassan Hazirah, Hatokova Zuzana, Hausenloy Derek J, Heales Simon JR, Hecker Matthias, Heiestad Christina, Hellgren Kim T, Henrique Alexandrino, Hepple Russell T, Hernansanz- Agustin Pablo, Hewakapuge Sudinna, Hickey Anthony J, Ho Dieu Hien, Hoehn Kyle L, Hoel Fredrik, Holland Olivia J, Holloway Graham P, Holzner Lorenz, Hoppel Charles L, Hoppel Florian, Hoppeler Hans, Houstek Josef, Huete-Ortega Maria, Hyrossova Petra, Iglesias-Gonzalez Javier, Indiveri Cesare, Irving Brian A, Isola Raffaella, Iyer Shilpa, Jackson Christopher Benjamin, Jadiya Pooja, Jana Prado Fabian, Jandeleit-Dahm Karin, Jang David H, Jang Young Charles, Janowska Joanna, Jansen Kirsten M, Jansen-Duerr Pidder, Jansone Baiba, Jarmuszkiewicz Wieslawa, Jaskiewicz Anna, Jaspers Richard T, Jedlicka Jan, Jerome Estaquier, Jespersen Nichlas Riise, Jha Rajan Kumar, Jones John G, Joseph Vincent, Juhasz Laszlo, Jurczak Michael J, Jurk Diana, Jusic Amela, Kaambre Tuuli, Kaczor Jan Jacek, Kainulainen Heikki, Kampa Rafal Pawel, Kandel Sunil Mani, Kane Daniel A, Kapferer Werner, Kapnick Senta, Kappler Lisa, Karabatsiakis Alexander, Karavaeva Iuliia, Karkucinska-Wieckowska Agnieszka, Kaur Sarbjot, Keijer Jaap, Keller Markus A, Keppner Gloria, Khamoui Andy V, Kidere Dita, Kilbaugh Todd, Kim Hyoung Kyu, Kim Julian KS, Kimoloi Sammy, Klepinin Aleksandr, Klepinina Lyudmila, Klingenspor Martin, Klocker Helmut, Kolassa Iris, Komlodi Timea, Koopman Werner JH, Kopitar-Jerala Natasa, Kowaltowski Alicia J, Kozlov Andrey V, Krajcova Adela, Krako Jakovljevic Nina, Kristal Bruce S, Krycer James R, Kuang Jujiao, Kucera Otto, Kuka Janis, Kwak Hyo Bum, Kwast Kurt E, Kwon Oh Sung, Laasmaa Martin, Labieniec-Watala Magdalena, Lagarrigue Sylviane, Lai Nicola, Lalic Nebojsa M, Land John M, Lane Nick, Laner Verena, Lanza Ian R, Laouafa Sofien, Laranjinha Joao, Larsen Steen, Larsen Terje S, Lavery Gareth G, Lazou Antigone, Ledo Ana Margarida, Lee Hong Kyu, Leeuwenburgh Christiaan, Lehti Maarit, Lemieux Helene, Lenaz Giorgio, Lerfall Joergen, Li Pingan Andy, Li Puma Lance, Liang Liping, Liepins Edgars, Lin Chien-Te, Liu Jiankang, Lopez Garcia Luis Carlos, Lucchinetti Eliana, Ma Tao, Macedo Maria Paula, Machado Ivo F, Maciej Sarah, MacMillan-Crow Lee Ann, Magalhaes Jose, Magri Andrea, Majtnerova Pavlina, Makarova Elina, Makrecka-Kuka Marina, Malik Afshan N, Marcouiller Francois, Marechal Amandine, Markova Michaela, Markovic Ivanka, Martin Daniel S, Martins Ana Dias, Martins Joao D, Maseko Tumisang Edward, Maull Felicia, Mazat Jean-Pierre, McKenna Helen T, McKenzie Matthew, McMillan Duncan GG, McStay Gavin P, Mendham Amy, Menze Michael A, Mercer John R, Merz Tamara, Messina Angela, Meszaros Andras, Methner Axel, Michalak Slawomir, Mila Guasch Maria, Minuzzi Luciele M, Misirkic Marjanovic Maja, Moellering Douglas R, Moisoi Nicoleta, Molina Anthony JA, Montaigne David, Moore Anthony L, Moore Christy, Moreau Kerrie, Moreira Bruno P, Moreno-Sanchez Rafael, Mracek Tomas, Muccini Anna Maria, Munro Daniel, Muntane Jordi, Muntean Danina M, Murray Andrew James, Musiol Eva, Nabben Miranda, Nair K Sreekumaran, Nehlin Jan O, Nemec Michal, Nesci Salvatore, Neufer P Darrell, Neuzil Jiri, Neviere Remi, Newsom Sean A, Norman Jennifer, Nozickova Katerina, Nunes Sara, Nuoffer Jean-Marc, O'Brien Kristin, O'Brien Katie A, O'Gorman Donal, Olgar Yusuf, Oliveira Ben, Oliveira Jorge, Oliveira Marcus F, Oliveira Marcos Tulio, Oliveira Pedro Fontes, Oliveira Paulo J, Olsen Rolf Erik, Orynbayeva Zulfiya, Osiewacz Heinz D, Paez Hector, Pak Youngmi Kim, Pallotta Maria Luigia, Palmeira Carlos, Parajuli Nirmala, Passos Joao F, Passrugger Manuela, Patel Hemal H, Pavlova Nadia, Pavlovic Kasja, Pecina Petr, Pedersen Tina M, Perales Jose Carles, Pereira da Silva Grilo da Silva Filomena, Pereira Rita, Pereira Susana P, Perez Valencia Juan Alberto, Perks Kara L, Pesta Dominik, Petit Patrice X, Pettersen Nitschke Ina Katrine, Pichaud Nicolas, Pichler Irene, Piel Sarah, Pietka Terri A, Pinho Sonia A, Pino Maria F, Pirkmajer Sergej, Place Nicolas, Plangger Mario, Porter Craig, Porter Richard K, Preguica Ines, Prigione Alessandro, Procaccio Vincent, Prochownik Edward V, Prola Alexandre, Pulinilkunnil Thomas, Puskarich Michael A, Puurand Marju, Radenkovic Filip, Ramzan Rabia, Rattan Suresh IS, Reano Simone, Reboredo-Rodriguez Patricia, Rees Bernard B, Renner-Sattler Kathrin, Rial Eduardo, Robinson Matthew M, Roden Michael, Rodrigues Ana Sofia, Rodriguez Enrique, Rodriguez-Enriquez Sara, Roesland Gro Vatne, Rohlena Jakub, Rolo Anabela Pinto, Ropelle Eduardo R, Roshanravan Baback, Rossignol Rodrigue, Rossiter Harry B, Rousar Tomas, Rubelj Ivica, Rybacka-Mossakowska Joanna, Saada Reisch Ann, Safaei Zahra, Salin Karine, Salvadego Desy, Sandi Carmen, Saner Nicholas, Santos Diana, Sanz Alberto, Sardao Vilma, Sarlak Saharnaz, Sazanov Leonid A, Scaife Paula, Scatena Roberto, Schartner Melanie, Scheibye-Knudsen Morten, Schilling Jan M, Schlattner Uwe, Schmitt Sabine, Schneider Gasser Edith Mariane, Schoenfeld Peter, Schots Pauke C, Schulz Rainer, Schwarzer Christoph, Scott Graham R, Selman Colin, Sendon Pamella Marie, Shabalina Irina G, Sharma Pushpa, Sharma Vipin, Shevchuk Igor, Shirazi Reza, Shiroma Jonathan G, Siewiera Karolina, Silber Ariel M, Silva Ana Maria, Sims Carrie A, Singer Dominique, Singh Brijesh Kumar, Skolik Robert A, Smenes Benedikte Therese, Smith James, Soares Felix Alexandre Antunes, Sobotka Ondrej, Sokolova Inna, Solesio Maria E, Soliz Jorge, Sommer Natascha, Sonkar Vijay K, Sova Marina, Sowton Alice P, Sparagna Genevieve C, Sparks Lauren M, Spinazzi Marco, Stankova Pavla, Starr Jonathan, Stary Creed, Stefan Eduard, Stelfa Gundega, Stepto Nigel K, Stevanovic Jelena, Stiban Johnny, Stier Antoine, Stocker Roland, Storder Julie, Sumbalova Zuzana, Suomalainen Anu, Suravajhala Prashanth, Svalbe Baiba, Swerdlow Russell H, Swiniuch Daria, Szabo Ildiko, Szewczyk Adam, Szibor Marten, Tanaka Masashi, Tandler Bernard, Tarnopolsky Mark A, Tausan Daniel, Tavernarakis Nektarios, Teodoro Joao Soeiro, Tepp Kersti, Thakkar Himani, Thapa Maheshwor, Thyfault John P, Tomar Dhanendra, Ton Riccardo, Torp May-Kristin, Torres-Quesada Omar, Towheed Atif, Treberg Jason R, Tretter Laszlo, Trewin Adam J, Trifunovic Aleksandra, Trivigno Catherine, Tronstad Karl Johan, Trougakos Ioannis P, Truu Laura, Tuncay Erkan, Turan Belma, Tyrrell Daniel J, Urban Tomas, Urner Sofia, Valentine Joseph Marco, Van Bergen Nicole J, Van der Ende Miranda, Varricchio Frederick, Vaupel Peter, Vella Joanna, Vendelin Marko, Vercesi Anibal E, Verdaguer Ignasi Bofill, Vernerova Andrea, Victor Victor Manuel, Vieira Ligo Teixeira Camila, Vidimce Josif, Viel Christian, Vieyra Adalberto, Vilks Karlis, Villena Josep A, Vincent Vinnyfred, Vinogradov Andrey D, Viscomi Carlo, Vitorino Rui Miguel Pinheiro, Vlachaki Walker Julia, Vogt Sebastian, Volani Chiara, Volska Kristine, Votion Dominique-Marie, Vujacic-Mirski Ksenija, Wagner Brett A, Ward Marie Louise, Warnsmann Verena, Wasserman David H, Watala Cezary, Wei Yau-Huei, Weinberger Klaus M, Weissig Volkmar, White Sarah Haverty, Whitfield Jamie, Wickert Anika, Wieckowski Mariusz R, Wiesner Rudolf J, Williams Caroline M, Winwood-Smith Hugh, Wohlgemuth Stephanie E, Wohlwend Martin, Wolff Jonci Nikolai, Wrutniak-Cabello Chantal, Wuest Rob CI, Yokota Takashi, Zablocki Krzysztof, Zanon Alessandra, Zanou Nadege, Zaugg Kathrin, Zaugg Michael, Zdrazilova Lucie, Zhang Yong, Zhang Yizhu, Zikova Alena, Zischka Hans, Zorzano Antonio, Zujovic Tijana, Zurmanova Jitka, Zvejniece Liga
- Subjects
uncoupling ,MitoPedia: Respiratory states, SI - The International System of Units, IUPAC, Coupling control, Mitochondrial preparations, Protonmotive force, Uncoupling, Oxidative phosphorylation, Phosphorylation efficiency, Electron transfer-pathway, LEAK-respiration, Residual oxygen consumption, Normalization of rate, Flow, Flux, Flux control ratio, Mitochondrial marker, Cell count, Oxygen ,[SDV]Life Sciences [q-bio] ,coupling control ,protonmotive force ,oxidative phosphorylation ,mitochondrial respiratory control ,State 4 ,electron transfer ,State 2 ,State 3 ,Mitochondrial physiology ,residual oxygen consumption ,flux ,normalization ,ion leak and slip compensatory state ,efficiency ,electron transfer system ,flow ,mitochondrial physiology ,oxygen ,mitochondrial preparations ,proton leak - Abstract
As the knowledge base and importance of mitochondrial physiology to evolution, health and diseaseexpands, the necessity for harmonizing the terminologyconcerning mitochondrial respiratory states and rates has become increasingly apparent. Thechemiosmotic theoryestablishes the mechanism of energy transformationandcoupling in oxidative phosphorylation. Theunifying concept of the protonmotive force providestheframeworkfordeveloping a consistent theoretical foundation ofmitochondrial physiology and bioenergetics.We followthe latest SI guidelines and those of the International Union of Pure and Applied Chemistry(IUPAC)onterminology inphysical chemistry, extended by considerationsofopen systems and thermodynamicsof irreversible processes.Theconcept-driven constructive terminology incorporates the meaning of each quantity and alignsconcepts and symbols withthe nomenclature of classicalbioenergetics. We endeavour to provide a balanced view ofmitochondrial respiratory control and a critical discussion on reporting data of mitochondrial respiration in terms of metabolic flows and fluxes.Uniform standards for evaluation of respiratory states and rates will ultimatelycontribute BEC 2020.1 doi:10.26124/bec:2020-0001.v1www.bioenergetics-communications.org3of 44to reproducibility between laboratories and thussupport the development of datarepositoriesof mitochondrial respiratory function in species, tissues, and cells.Clarity of concept and consistency of nomenclature facilitate effective transdisciplinary communication, education, and ultimately further discovery.
- Published
- 2020
23. Characterization of glutamate transport in isolated adult rat heart cells
- Author
-
Dinkelborg, Ludger M., Wiesner, Rudolf J., Grieshaber, Manfred K., Lubec, Gert, editor, and Rosenthal, Gerald A., editor
- Published
- 1990
- Full Text
- View/download PDF
24. Isolation of functional pure mitochondria by superparamagnetic microbeads
- Author
-
Hornig-Do, Hue-Tran, Günther, Gritt, Bust, Maria, Lehnartz, Patricia, Bosio, Andreas, and Wiesner, Rudolf J.
- Published
- 2009
- Full Text
- View/download PDF
25. Methionine restriction slows down senescence in human diploid fibroblasts
- Author
-
Kozieł, Rafał, Ruckenstuhl, Christoph, Albertini, Eva, Neuhaus, Michael, Netzberger, Christine, Bust, Maria, Madeo, Frank, Wiesner, Rudolf J., and Jansen-Dürr, Pidder
- Published
- 2014
- Full Text
- View/download PDF
26. Mitochondrial membrane proteins and VPS35 orchestrate selective removal of mtDNA
- Author
-
Pla-Martin, David, primary, Sen, Ayesha, additional, Kallabis, Sebastian, additional, Nüchel, Julian, additional, Maliphol, Kanjanamas, additional, Hofmann, Julia, additional, Krüger, Marcus, additional, and Wiesner, Rudolf J., additional
- Published
- 2021
- Full Text
- View/download PDF
27. Selective Neuron Vulnerability in Common and Rare Diseases—Mitochondria in the Focus
- Author
-
Paß, Thomas, primary, Wiesner, Rudolf J., additional, and Pla-Martín, David, additional
- Published
- 2021
- Full Text
- View/download PDF
28. Zusammenhänge zwischen mitochondrialen Myopathien und Sarkopenie
- Author
-
Brunn, Anna Gertrud, Zentrum Physiologie Und Pathophysiologie (Köln), Oexner, Rafael Rudolf, and Wiesner, Rudolf J.
- Subjects
Medizin und Gesundheit - Published
- 2021
- Full Text
- View/download PDF
29. Ventrale oder dorsale Operationsverfahren
- Author
-
Kiskämper, Anna, Stein, Gregor, Universitätsklinikum Köln. Klinik Und Poliklinik Für Orthopädie Und Unfallchirurgie, and Wiesner, Rudolf J.
- Published
- 2021
- Full Text
- View/download PDF
30. Author Response: K320E-Twinkle(skm) Mice Are Genetically Heterogeneous for Secondary mtDNA Deletions Impairing Comparison With Controls
- Author
-
Kimoloi, Sammy, Pla-Martin, David, Oexner, Rafael R., Baris, Olivier R., Wiesner, Rudolf J., Kimoloi, Sammy, Pla-Martin, David, Oexner, Rafael R., Baris, Olivier R., and Wiesner, Rudolf J.
- Published
- 2021
31. Selective Neuron Vulnerability in Common and Rare Diseases-Mitochondria in the Focus
- Author
-
Pass, Thomas, Wiesner, Rudolf J., Pla-Martin, David, Pass, Thomas, Wiesner, Rudolf J., and Pla-Martin, David
- Abstract
Mitochondrial dysfunction is a central feature of neurodegeneration within the central and peripheral nervous system, highlighting a strong dependence on proper mitochondrial function of neurons with especially high energy consumptions. The fitness of mitochondria critically depends on preservation of distinct processes, including the maintenance of their own genome, mitochondrial dynamics, quality control, and Ca2+ handling. These processes appear to be differently affected in common neurodegenerative diseases, such as Alzheimer's and Parkinson's disease, as well as in rare neurological disorders, including Huntington's disease, Amyotrophic Lateral Sclerosis and peripheral neuropathies. Strikingly, particular neuron populations of different morphology and function perish in these diseases, suggesting that cell-type specific factors contribute to the vulnerability to distinct mitochondrial defects. Here we review the disruption of mitochondrial processes in common as well as in rare neurological disorders and its impact on selective neurodegeneration. Understanding discrepancies and commonalities regarding mitochondrial dysfunction as well as individual neuronal demands will help to design new targets and to make use of already established treatments in order to improve treatment of these diseases.
- Published
- 2021
32. Nonsense mutations in the COX1 subunit impair the stability of respiratory chain complexes rather than their assembly
- Author
-
Hornig‐Do, Hue‐Tran, Tatsuta, Takashi, Buckermann, Angela, Bust, Maria, Kollberg, Gittan, Rötig, Agnes, Hellmich, Martin, Nijtmans, Leo, and Wiesner, Rudolf J
- Published
- 2012
- Full Text
- View/download PDF
33. Catecholamine metabolism drives generation of mitochondrial DNA deletions in dopaminergic neurons
- Author
-
Neuhaus, Johannes F.G., Baris, Olivier R., Hess, Simon, Moser, Natasha, Schröder, Hannsjörg, Chinta, Shankar J., Andersen, Julie K., Kloppenburg, Peter, and Wiesner, Rudolf J.
- Published
- 2014
- Full Text
- View/download PDF
34. Increased Ca2+ sensitivity and protein expression of SERCA 2a in situations of chronic β3-adrenoceptor deficiency
- Author
-
Ziskoven, Christoph, Grafweg, Sabrina, Bölck, Birgit, Wiesner, Rudolf J., Jimenez, Maria, Giacobino, Jean-Paul, Bloch, W., Schwinger, Robert H. G., and Brixius, Klara
- Published
- 2007
- Full Text
- View/download PDF
35. Einflüsse der Baroreflex-Aktivierungstherapie auf Blutdruck und Hospitalisierungsrate bei Patienten mit therapierefraktärer arterieller Hypertonie
- Author
-
Halbach, Marcel Daniel, Universitätsklinikum Köln. Klinik Und Poliklinik Für Kardiologie, Pneumologie, Grothaus, David, and Wiesner, Rudolf J.
- Subjects
Medizin und Gesundheit - Published
- 2020
- Full Text
- View/download PDF
36. α-Actinin 4 and BAT1 interaction with the Cytochrome c promoter upon skeletal muscle differentiation
- Author
-
Goffart, Steffi, Franko, Andras, Clemen, Christoph S., and Wiesner, Rudolf J.
- Published
- 2006
- Full Text
- View/download PDF
37. Mitochondrial Dysfunction Combined with High Calcium Load Leads to Impaired Antioxidant Defense Underlying the Selective Loss of Nigral Dopaminergic Neurons
- Author
-
Ricke, Konrad M., Pass, Thomas, Kimoloi, Sammy, Faehrmann, Kai, Juengst, Christian, Schauss, Astrid, Baris, Olivier R., Aradjanski, Marijana, Trifunovic, Aleksandra, Faelker, Therese M. Eriksson, Bergami, Matteo, Wiesner, Rudolf J., Ricke, Konrad M., Pass, Thomas, Kimoloi, Sammy, Faehrmann, Kai, Juengst, Christian, Schauss, Astrid, Baris, Olivier R., Aradjanski, Marijana, Trifunovic, Aleksandra, Faelker, Therese M. Eriksson, Bergami, Matteo, and Wiesner, Rudolf J.
- Abstract
Mitochondrial dysfunction is critically involved in Parkinson's disease, characterized by loss of dopaminergic neurons (DaNs) in the substantia nigra (SNc), whereas DaNs in the neighboring ventral tegmental area (VTA) are much less affected. In contrast to VTA, SNc DaNs engage calcium channels to generate action potentials, which lead to oxidant stress by yet unknown pathways. To determine the molecular mechanisms linking calcium load with selective cell death in the presence of mitochondrial deficiency, we analyzed the mitochondrial redox state and the mitochondrial membrane potential in mice of both sexes with genetically induced, severe mitochondrial dysfunction in DaNs (MitoPark mice), at the same time expressing a redox-sensitive GFP targeted to the mitochondrial matrix. Despite mitochondrial insufficiency in all DaNs, exclusively SNc neurons showed an oxidized redox-system, i.e., a low reduced/oxidized glutathione (GSH-GSSG) ratio. This was mimicked by cyanide, but not by rotenone or antimycin A, making the involvement of reactive oxygen species rather unlikely. Surprisingly, a high mitochondrial inner membrane potential was maintained in MitoPark SNc DaNs. Antagonizing calcium influx into the cell and into mitochondria, respectively, rescued the disturbed redox ratio and induced further hyperpolarization of the inner mitochondrial membrane. Our data therefore show that the constant calcium load in SNc DaNs is counterbalanced by a high mitochondrial inner membrane potential, even under conditions of severe mitochondrial dysfunction, but triggers a detrimental imbalance in the mitochondrial redox system, which will lead to neuron death. Our findings thus reveal a new mechanism, redox imbalance, which underlies the differential vulnerability of DaNs to mitochondrial defects.
- Published
- 2020
38. The Impact of Mitochondrial Dysfunction on Dopaminergic Neurons in the Olfactory Bulb and Odor Detection
- Author
-
Pass, Thomas, Assfalg, Marlene, Tolve, Marianna, Blaess, Sandra, Rothermel, Markus, Wiesner, Rudolf J., Ricke, Konrad M., Pass, Thomas, Assfalg, Marlene, Tolve, Marianna, Blaess, Sandra, Rothermel, Markus, Wiesner, Rudolf J., and Ricke, Konrad M.
- Abstract
Understanding non-motor symptoms of Parkinson's disease is important in order to unravel the underlying molecular mechanisms of the disease. Olfactory dysfunction is an early stage, non-motor symptom which occurs in 95% of Parkinson's disease patients. Mitochondrial dysfunction is a key feature in Parkinson's disease and importantly contributes to the selective loss of dopaminergic neurons thesubstantia nigra pars compacta. The olfactory bulb, the first olfactory processing station, also contains dopaminergic neurons, which modulate odor information and thereby enable odor detection as well as odor discrimination. MitoPark mice are a genetic model for Parkinson's disease with severe mitochondrial dysfunction, reproducing the differential vulnerability of dopaminergic neurons in the midbrain. These animals were used to investigate the impact of mitochondrial dysfunction on olfactory-related behavior and olfactory bulb dopaminergic neuron survival. Odor detection was severely impaired in MitoPark mice. Interestingly, only the small anaxonic dopaminergic subpopulation, which is continuously replenished by neurogenesis, was moderately reduced in number, much less compared with dopaminergic neurons in the midbrain. As a potential compensatory response, an enhanced mobilization of progenitor cells was found in the subventricular zone. These results reveal a high robustness of dopaminergic neurons located in the olfactory bulb towards mitochondrial impairment, in striking contrast to their midbrain counterparts.
- Published
- 2020
39. Extraocular Muscle Reveals Selective Vulnerability of Type IIB Fibers to Respiratory Chain Defects Induced by Mitochondrial DNA Alterations
- Author
-
Oexner, Rafael R., Pla-Martin, David, Pass, Thomas, Wiesen, Martin H. J., Zentis, Peter, Schauss, Astrid, Baris, Olivier R., Kimoloi, Sammy, Wiesner, Rudolf J., Oexner, Rafael R., Pla-Martin, David, Pass, Thomas, Wiesen, Martin H. J., Zentis, Peter, Schauss, Astrid, Baris, Olivier R., Kimoloi, Sammy, and Wiesner, Rudolf J.
- Abstract
PURPOSE. The purpose of this study was to gain insights on the pathogenesis of chronic progressive external ophthalmoplegia, thus we investigated the vulnerability of five extra ocular muscles (EOMs) fiber types to pathogenic mitochondrial DNA deletions in a mouse model expressing a mutated mitochondrial helicase TWINKLE. METHODS. Consecutive pairs of EOM sections were analyzed by cytochrome C oxidase (COX)/succinate dehydrogenase (SDH) assay and fiber type specific immunohistochemistry (type I, IIA, IIB, embryonic, and EOM-specific staining). RESULTS. The mean average of COX deficient fibers (COX-) in the recti muscles of mutant mice was 1.04 +/- 0.52% at 12 months and increased with age (7.01 +/- 1.53% at 24 months). A significant proportion of these COX-fibers were of the fast-twitch, glycolytic type IIB (> 50% and > 35% total COX-fibers at 12 and 24 months, respectively), whereas embryonic myosin heavy chain-expressing fibers were almost completely spared. Furthermore, the proportion of COX-fibers in the type IIB-rich retractor bulbi muscle was > 2-fold higher compared to the M. recti at both 12 (2.6 +/- 0.78%) and 24 months (20.85 +/- 2.69%). Collectively, these results demonstrate a selective vulnerability of type IIB fibers to mitochondrial DNA (mtDNA) deletions in EOMs and retractor bulbi muscle. We also show that EOMs of mutant mice display histopathological abnormalities, including altered fiber type composition, increased fibrosis, ragged red fibers, and infiltration of mononucleated nonmuscle cells. CONCLUSIONS. Our results point to the existence of fiber type IIB-intrinsic factors and/or molecular mechanisms that predispose them to increased generation, clonal expansion, and detrimental effects of mtDNA deletions.
- Published
- 2020
40. Accurate mapping of mitochondrial DNA deletions and duplications using deep sequencing
- Author
-
Basu, Swaraj, Xie, Xie, Uhler, Jay P., Hedberg-Oldfors, Carola, Milenkovic, Dusanka, Baris, Olivier R., Kimoloi, Sammy, Matic, Stanka, Stewart, James B., Larsson, Nils-Goran, Wiesner, Rudolf J., Oldfors, Anders, Gustafsson, Claes M., Falkenberg, Maria, Larsson, Erik, Basu, Swaraj, Xie, Xie, Uhler, Jay P., Hedberg-Oldfors, Carola, Milenkovic, Dusanka, Baris, Olivier R., Kimoloi, Sammy, Matic, Stanka, Stewart, James B., Larsson, Nils-Goran, Wiesner, Rudolf J., Oldfors, Anders, Gustafsson, Claes M., Falkenberg, Maria, and Larsson, Erik
- Abstract
Deletions and duplications in mitochondrial DNA (mtDNA) cause mitochondrial disease and accumulate in conditions such as cancer and age-related disorders, but validated high-throughput methodology that can readily detect and discriminate between these two types of events is lacking. Here we establish a computational method, MitoSAlt, for accurate identification, quantification and visualization of mtDNA deletions and duplications from genomic sequencing data. Our method was tested on simulated sequencing reads and human patient samples with single deletions and duplications to verify its accuracy. Application to mouse models of mtDNA maintenance disease demonstrated the ability to detect deletions and duplications even at low levels of heteroplasmy. Author summary Deletions in the mitochondrial genome cause a wide variety of rare disorders, but are also linked to more common conditions such as neurodegeneration, diabetes type 2, and the normal ageing process. There is also a growing awareness that mtDNA duplications, which are also relevant for human disease, may be more common than previously thought. Despite their clinical importance, our current knowledge about the abundance, characteristics and diversity of mtDNA deletions and duplications is fragmented, and based to large extent on a limited view provided by traditional low-throughput analyses. Here, we describe a bioinformatics method, MitoSAlt, that can accurately map and classify mtDNA deletions and duplications using high-throughput sequencing. Application of this methodology to mouse models of mitochondrial deficiencies revealed a large number of duplications, suggesting that these may previously have been underestimated.
- Published
- 2020
41. Mitochondrial electron transport chain activity is not involved in ultraviolet A (UVA)-induced cell death
- Author
-
Schauen, Matthias, Hornig-Do, Hue-Tran, Schomberg, Sarah, Herrmann, Gernot, and Wiesner, Rudolf J.
- Published
- 2007
- Full Text
- View/download PDF
42. Mitochondrial function is essential for humoral immunity by controlling flux of the TCA cycle, phosphatidic acid and mTOR activity in B cells
- Author
-
Urbanczyk, Sophia, primary, Baris, Olivier R., additional, Hofmann, Jörg, additional, Golombek, Florian, additional, Castiglione, Kathrin, additional, Meng, Xianyi, additional, Bozec, Aline, additional, Mougiakakos, Dimitrios, additional, Schulz, Sebastian R., additional, Schuh, Wolfgang, additional, Schlötzer-Schrehardt, Ursula, additional, Steinmetz, Tobit D., additional, Brodesser, Susanne, additional, Wiesner, Rudolf J., additional, and Mielenz, Dirk, additional
- Published
- 2021
- Full Text
- View/download PDF
43. Author Response: K320E-Twinkleskm Mice Are Genetically Heterogeneous for Secondary mtDNA Deletions Impairing Comparison With Controls
- Author
-
Kimoloi, Sammy, primary, Pla-Martín, David, additional, Oexner, Rafael R., additional, Baris, Olivier R., additional, and Wiesner, Rudolf J., additional
- Published
- 2021
- Full Text
- View/download PDF
44. Accurate mapping of mitochondrial DNA deletions and duplications using deep sequencing
- Author
-
Basu, Swaraj, primary, Xie, Xie, additional, Uhler, Jay P., additional, Hedberg-Oldfors, Carola, additional, Milenkovic, Dusanka, additional, Baris, Olivier R., additional, Kimoloi, Sammy, additional, Matic, Stanka, additional, Stewart, James B., additional, Larsson, Nils-Göran, additional, Wiesner, Rudolf J., additional, Oldfors, Anders, additional, Gustafsson, Claes M., additional, Falkenberg, Maria, additional, and Larsson, Erik, additional
- Published
- 2020
- Full Text
- View/download PDF
45. Negative regulation of mitochondrial transcription by mitochondrial topoisomerase I
- Author
-
Sobek, Stefan, Dalla Rosa, Ilaria, Pommier, Yves, Bornholz, Beatrice, Kalfalah, Faiza, Zhang, Hongliang, Wiesner, Rudolf J., von Kleist-Retzow, Jürgen-Christoph, Hillebrand, Frank, Schaal, Heiner, Mielke, Christian, Christensen, Morten O., and Boege, Fritz
- Published
- 2013
- Full Text
- View/download PDF
46. Proliferation of Mitochondria in Chronically Stimulated Rabbit Skeletal Muscle—Transcription of Mitochondrial Genes and Copy Number of Mitochondrial DNA
- Author
-
Schultz, Jeanette and Wiesner, Rudolf J.
- Published
- 2000
- Full Text
- View/download PDF
47. Predominant activation of endothelin-dependent cardiac hypertrophy by norepinephrine in rat left ventricle
- Author
-
Moser, Lutz, Faulhaber, Jorg, Wiesner, Rudolf J., and Ehmke, Heimo
- Subjects
Endothelin -- Physiological aspects ,Heart ventricle, Left -- Research ,Heart enlargement -- Physiological aspects ,Noradrenaline -- Physiological aspects ,Biological sciences - Abstract
Locally released endothelin (ET)-1 has been recently identified as an important mediator of cardiac hypertrophy. It is still unclear, however, which primary stimulus specifically activates ET-dependent signaling pathways. We therefore examined in adult rats (n = 51) the effects of a selective E[T.sub.A] receptor antagonist in experimental models of cardiac hypertrophy, in which myocardial growth is predominantly initiated by a single primary stimulus. Rats were exposed to mechanical overload (ascending aortic stenosis), increased levels of circulating ANG II (ANG II infusion combined with hydralazine), or adrenergic stimulation (infusion of norepinephrine in a subpressor dose) for 7 days. All experimental treatments significantly increased left ventricular weight/body weight ratios compared with untreated rats, whereas systolic left ventricular peak pressure was increased only after ascending aortic stenosis. E[T.sub.A] receptor blockade exclusively reduced norepinephrine-induced cardiac hypertrophy and atrial natriuretic peptide gene expression. Blood pressure levels and heart rates remained unaffected during E[T.sub.A] receptor blockade in all experimental groups. These data indicate that in rat left ventricle, the ET-dependent signaling pathway leading to early development of cardiac hypertrophy and fetal gene expression is primarily activated by norepinephrine. angiotensin II; endothelin-A receptor; gene expression; norepinephrine; remodeling
- Published
- 2002
48. Stimulation of Mitochondrial Gene Expression and Proliferation of Mitochondria Following Impairment of Cellular Energy Transfer by Inhibition of the Phosphocreatine Circuit in Rat Hearts
- Author
-
Wiesner, Rudolf J., Hornung, Till V., Garman, J. David, Clayton, David A., O'Gorman, Eddie, and Wallimann, Theo
- Published
- 1999
- Full Text
- View/download PDF
49. Extraocular Muscle Reveals Selective Vulnerability of Type IIB Fibers to Respiratory Chain Defects Induced by Mitochondrial DNA Alterations
- Author
-
Oexner, Rafael R., primary, Pla-Martín, David, additional, Paß, Thomas, additional, Wiesen, Martin H. J., additional, Zentis, Peter, additional, Schauss, Astrid, additional, Baris, Olivier R., additional, Kimoloi, Sammy, additional, and Wiesner, Rudolf J., additional
- Published
- 2020
- Full Text
- View/download PDF
50. Mitochondrial DNA mutations induce mitochondrial biogenesis and increase the tumorigenic potential of Hodgkin and Reed–Sternberg cells
- Author
-
Haumann, Sophie, primary, Boix, Julia, additional, Knuever, Jana, additional, Bieling, Angela, additional, Vila Sanjurjo, Anton, additional, Elson, Joanna L, additional, Blakely, Emma L, additional, Taylor, Robert W, additional, Riet, Nicole, additional, Abken, Hinrich, additional, Kashkar, Hamid, additional, Hornig-Do, Hue-Tran, additional, and Wiesner, Rudolf J, additional
- Published
- 2020
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.