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229 results on '"Wüst, Rob C. I."'

5. Smoking cessation only partially reverses cardiac metabolic and structural remodeling in mice

Author

Aid, Jekaterina, Tanjeko, Ajime Tom, Serré, Jef, Eggelbusch, Moritz, Noort, Wendy, de Wit, Gerard M J, van Weeghel, Michel, Puurand, Marju, Tepp, Kersti, Gayan-Ramirez, Ghislaine, Degens, Hans, Käämbre, Tuuli, Wüst, Rob C I, Aid, Jekaterina, Tanjeko, Ajime Tom, Serré, Jef, Eggelbusch, Moritz, Noort, Wendy, de Wit, Gerard M J, van Weeghel, Michel, Puurand, Marju, Tepp, Kersti, Gayan-Ramirez, Ghislaine, Degens, Hans, Käämbre, Tuuli, and Wüst, Rob C I

Abstract

Aims: Active cigarette smoking is a major risk factor for chronic obstructive pulmonary disease that remains elevated after cessation. Skeletal muscle dysfunction has been well documented after smoking, but little is known about cardiac adaptations to cigarette smoking. The underlying cellular and molecular cardiac adaptations, independent of confounding lifestyle factors, and time course of reversibility by smoking cessation remain unclear. We hypothesized that smoking negatively affects cardiac metabolism and induces local inflammation in mice, which do not readily reverse upon 2-week smoking cessation. Methods: Mice were exposed to air or cigarette smoke for 14 weeks with or without 1- or 2-week smoke cessation. We measured cardiac mitochondrial respiration by high-resolution respirometry, cardiac mitochondrial density, abundance of mitochondrial supercomplexes by electrophoresis, and capillarization, fibrosis, and macrophage infiltration by immunohistology, and performed cardiac metabolome and lipidome analysis by mass spectrometry. Results: Mitochondrial protein, supercomplex content, and respiration (all p < 0.03) were lower after smoking, which were largely reversed within 2-week smoking cessation. Metabolome and lipidome analyses revealed alterations in mitochondrial metabolism, a shift from fatty acid to glucose metabolism, which did not revert to control upon smoking cessation. Capillary density was not different after smoking but increased after smoking cessation (p = 0.02). Macrophage infiltration and fibrosis (p < 0.04) were higher after smoking but did not revert to control upon smoking cessation. Conclusions: While cigarette-impaired smoking-induced cardiac mitochondrial function was reversed by smoking cessation, the remaining fibrosis and macrophage infiltration may contribute to the increased risk of cardiovascular events after smoking cessation.

Published
2024

9. Cellular, mitochondrial and molecular alterations associate with early left ventricular diastolic dysfunction in a porcine model of diabetic metabolic derangement

Author

Heinonen, Ilkka, Sorop, Oana, van Dalen, Bas M., Wüst, Rob C. I., van de Wouw, Jens, de Beer, Vincent J., Octavia, Yanti, van Duin, Richard W. B., Hoogstrate, Youri, Blonden, Lau, Alkio, Milla, Anttila, Katja, Stubbs, Andrew, van der Velden, Jolanda, Merkus, Daphne, and Duncker, Dirk J.

Published
2020
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11. Mitochondrial dysfunction in human hypertrophic cardiomyopathy is linked to cardiomyocyte architecture disruption and corrected by improving NADH-driven mitochondrial respiration

Author

Nollet, Edgar E, primary, Duursma, Inez, additional, Rozenbaum, Anastasiya, additional, Eggelbusch, Moritz, additional, Wüst, Rob C I, additional, Schoonvelde, Stephan A C, additional, Michels, Michelle, additional, Jansen, Mark, additional, van der Wel, Nicole N, additional, Bedi, Kenneth C, additional, Margulies, Kenneth B, additional, Nirschl, Jeff, additional, Kuster, Diederik W D, additional, and van der Velden, Jolanda, additional

Published
2023
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13. Longitudinal CMR assessment of cardiac global longitudinal strain and hemodynamic forces in a mouse model of heart failure

Author

Daal, Mariah R. R., Strijkers, Gustav J., Hautemann, David J., Nederveen, Aart J., Wüst, Rob C. I., and Coolen, Bram F.

Abstract

To longitudinally assess left ventricle (LV) global longitudinal strain (GLS) and hemodynamic forces during the early stages of cardiac dysfunction in a mouse model of heart failure with preserved ejection fraction (HFpEF). Cardiac MRI measurements were performed in control mice (n = 6), and db/db mice (n = 7), whereby animals were scanned four times between the age of 11–15 weeks. After the first scan, the db/db animals received a doxycycline intervention to accelerate progression of HFpEF. Systolic function was evaluated based on a series of prospectively ECG-triggered short-axis CINE images acquired from base to apex. Cardiac GLS and hemodynamic forces values were evaluated based on high frame rate retrospectively gated 2-, 3-, and 4-chamber long-axis CINE images. Ejection fraction (EF) was not different between control and db/db animals, despite that cardiac output, as well as end systolic and end diastolic volume were significantly higher in control animals. Whereas GLS parameters were not significantly different between groups, hemodynamic force root mean square (RMS) values, as well as average hemodynamic forces and the ratio between hemodynamic forces in the inferolateral-anteroseptal and apical–basal direction were lower in db/db mice compared to controls. More importantly, hemodynamic forces parameters showed a significant interaction effect between time and group. Our results indicated that hemodynamic forces parameters were the only functional outcome measure that showed distinct temporal differences between groups. As such, changes in hemodynamic forces reflect early alterations in cardiac function which can be of added value in (pre)clinical research on HFpEF.

Published
2024
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17. TMBIM5 loss of function alters mitochondrial matrix ion homeostasis and causes a skeletal myopathy

Author

Zhang, Li, Dietsche, Felicia, Seitaj, Bruno; https://orcid.org/0000-0002-4116-2685, Rojas-Charry, Liliana, Latchman, Nadina, Tomar, Dhanendra; https://orcid.org/0000-0002-3144-7257, Wüst, Rob C I; https://orcid.org/0000-0003-3781-5177, Nickel, Alexander, Frauenknecht, Katrin B M; https://orcid.org/0000-0002-1372-3297, Schoser, Benedikt, Schumann, Sven; https://orcid.org/0000-0003-1785-622X, Schmeisser, Michael J; https://orcid.org/0000-0002-5514-1922, vom Berg, Johannes; https://orcid.org/0000-0002-4086-1564, Buch, Thorsten; https://orcid.org/0000-0002-2236-9074, Finger, Stefanie; https://orcid.org/0000-0002-1967-1715, Wenzel, Philip, Maack, Christoph, Elrod, John W; https://orcid.org/0000-0003-3925-2224, Parys, Jan B; https://orcid.org/0000-0002-3591-4967, Bultynck, Geert; https://orcid.org/0000-0002-5968-4828, Methner, Axel; https://orcid.org/0000-0002-8774-0057, Zhang, Li, Dietsche, Felicia, Seitaj, Bruno; https://orcid.org/0000-0002-4116-2685, Rojas-Charry, Liliana, Latchman, Nadina, Tomar, Dhanendra; https://orcid.org/0000-0002-3144-7257, Wüst, Rob C I; https://orcid.org/0000-0003-3781-5177, Nickel, Alexander, Frauenknecht, Katrin B M; https://orcid.org/0000-0002-1372-3297, Schoser, Benedikt, Schumann, Sven; https://orcid.org/0000-0003-1785-622X, Schmeisser, Michael J; https://orcid.org/0000-0002-5514-1922, vom Berg, Johannes; https://orcid.org/0000-0002-4086-1564, Buch, Thorsten; https://orcid.org/0000-0002-2236-9074, Finger, Stefanie; https://orcid.org/0000-0002-1967-1715, Wenzel, Philip, Maack, Christoph, Elrod, John W; https://orcid.org/0000-0003-3925-2224, Parys, Jan B; https://orcid.org/0000-0002-3591-4967, Bultynck, Geert; https://orcid.org/0000-0002-5968-4828, and Methner, Axel; https://orcid.org/0000-0002-8774-0057

Abstract

Ion fluxes across the inner mitochondrial membrane control mitochondrial volume, energy production, and apoptosis. TMBIM5, a highly conserved protein with homology to putative pH-dependent ion channels, is involved in the maintenance of mitochondrial cristae architecture, ATP production, and apoptosis. Here, we demonstrate that overexpressed TMBIM5 can mediate mitochondrial calcium uptake. Under steady-state conditions, loss of TMBIM5 results in increased potassium and reduced proton levels in the mitochondrial matrix caused by attenuated exchange of these ions. To identify the in vivo consequences of TMBIM5 dysfunction, we generated mice carrying a mutation in the channel pore. These mutant mice display increased embryonic or perinatal lethality and a skeletal myopathy which strongly correlates with tissue-specific disruption of cristae architecture, early opening of the mitochondrial permeability transition pore, reduced calcium uptake capability, and mitochondrial swelling. Our results demonstrate that TMBIM5 is an essential and important part of the mitochondrial ion transport system machinery with particular importance for embryonic development and muscle function.

Published
2022

19. Tissue‐specific effects of exercise as NAD+‐boosting strategy: Current knowledge and future perspectives.

Author

Walzik, David, Jonas, Wiebke, Joisten, Niklas, Belen, Sergen, Wüst, Rob C. I., Guillemin, Gilles, and Zimmer, Philipp

Subjects
ENERGY metabolism, EXERCISE therapy, ENZYME metabolism, ENERGY consumption, CELL physiology
Abstract

Nicotinamide adenine dinucleotide (NAD+) is an evolutionarily highly conserved coenzyme with multi‐faceted cell functions, including energy metabolism, molecular signaling processes, epigenetic regulation, and DNA repair. Since the discovery that lower NAD+ levels are a shared characteristic of various diseases and aging per se, several NAD+‐boosting strategies have emerged. Other than pharmacological and nutritional approaches, exercise is thought to restore NAD+ homeostasis through metabolic adaption to chronically recurring states of increased energy demand. In this review we discuss the impact of acute exercise and exercise training on tissue‐specific NAD+ metabolism of rodents and humans to highlight the potential value as NAD+‐boosting strategy. By interconnecting results from different investigations, we aim to draw attention to tissue‐specific alterations in NAD+ metabolism and the associated implications for whole‐body NAD+ homeostasis. Acute exercise led to profound alterations of intracellular NAD+ metabolism in various investigations, with the magnitude and direction of changes being strongly dependent on the applied exercise modality, cell type, and investigated animal model or human population. Exercise training elevated NAD+ levels and NAD+ metabolism enzymes in various tissues. Based on these results, we discuss molecular mechanisms that might connect acute exercise‐induced disruptions of NAD+/NADH homeostasis to chronic exercise adaptions in NAD+ metabolism. Taking this hypothesis‐driven approach, we hope to inspire future research on the molecular mechanisms of exercise as NAD+‐modifying lifestyle intervention, thereby elucidating the potential therapeutic value in NAD+‐related pathologies. [ABSTRACT FROM AUTHOR]

Published
2023
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24. TMBIM5 loss of function alters mitochondrial matrix ion homeostasis and causes a skeletal myopathy.

Author

Li Zhang, Dietsche, Felicia, Seitaj, Bruno, Rojas-Charry, Liliana, Latchman, Nadina, Tomar, Dhanendra, Wüst, Rob C. I., Nickel, Alexander, Frauenknecht, Katrin B. M., Schoser, Benedikt, Schumann, Sven, Schmeisser, Michael J., vom Berg, Johannes, Buch, Thorsten, Finger, Stefanie, Wenzel, Philip, Maack, Christoph, Elrod, John W., Parys, Jan B., and Bultynck, Geert

Published
2022
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30. The Antibiotic Doxycycline Impairs Cardiac Mitochondrial and Contractile Function

Author

Wüst, Rob C. I., primary, Coolen, Bram F., additional, Held, Ntsiki M., additional, Daal, Mariah R. R., additional, Alizadeh Tazehkandi, Vida, additional, Baks-te Bulte, Luciënne, additional, Wiersma, Marit, additional, Kuster, Diederik W. D., additional, Brundel, Bianca J. J. M., additional, van Weeghel, Michel, additional, Strijkers, Gustav J., additional, and Houtkooper, Riekelt H., additional

Published
2021
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32. Time‐restricted feeding during the inactive phase abolishes the daily rhythm in mitochondrial respiration in rat skeletal muscle.

Author

de Goede, Paul, Wüst, Rob C. I., Schomakers, Bauke V., Denis, Simone, Vaz, Frédéric M., Pras‐Raves, Mia L., van Weeghel, Michel, Yi, Chun‐Xia, Kalsbeek, Andries, and Houtkooper, Riekelt H.

Abstract

Shift‐workers show an increased incidence of type 2 diabetes mellitus (T2DM). A possible mechanism is the disruption of the circadian timing of glucose homeostasis. Skeletal muscle mitochondrial function is modulated by the molecular clock. We used time‐restricted feeding (TRF) during the inactive phase to investigate how mistimed feeding affects muscle mitochondrial metabolism. Rats on an ad libitum (AL) diet were compared to those that could eat only during the light (inactive) or dark (active) phase. Mitochondrial respiration, metabolic gene expressions, and metabolite concentrations were determined in the soleus muscle. Rats on AL feeding or dark‐fed TRF showed a clear daily rhythm in muscle mitochondrial respiration. This rhythm in mitochondrial oxidative phosphorylation capacity was abolished in light‐fed TRF animals and overall 24h respiration was lower. The expression of several genes involved in mitochondrial biogenesis and the fission/fusion machinery was altered in light‐fed animals. Metabolomics analysis indicated that light‐fed animals had lost rhythmic levels of α‐ketoglutarate and citric acid. Contrastingly, lipidomics showed that light‐fed animals abundantly gained rhythmicity in levels of triglycerides. Furthermore, while the RER shifted entirely with the food intake in the light‐fed animals, many measured metabolic parameters (e.g., activity and mitochondrial respiration) did not strictly align with the shifted timing of food intake, resulting in a mismatch between expected metabolic supply/demand (as dictated by the circadian timing system and light/dark‐cycle) and the actual metabolic supply/demand (as dictated by the timing of food intake). These data suggest that shift‐work impairs mitochondrial metabolism and causes metabolic inflexibility, which can predispose to T2DM. [ABSTRACT FROM AUTHOR]

Published
2022
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37. Electrophysiological Abnormalities in VLCAD Deficient hiPSC-Cardiomyocytes Can Be Improved by Lowering Accumulation of Fatty Acid Oxidation Intermediates

Author

Knottnerus, Suzan J. G., primary, Mengarelli, Isabella, additional, Wüst, Rob C. I., additional, Baartscheer, Antonius, additional, Bleeker, Jeannette C., additional, Coronel, Ruben, additional, Ferdinandusse, Sacha, additional, Guan, Kaomei, additional, IJlst, Lodewijk, additional, Li, Wener, additional, Luo, Xiaojing, additional, Portero, Vincent M., additional, Ulbricht, Ying, additional, Visser, Gepke, additional, Wanders, Ronald J. A., additional, Wijburg, Frits A., additional, Verkerk, Arie O., additional, Houtkooper, Riekelt H., additional, and Bezzina, Connie R., additional

Published
2020
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38. Nutritional ketosis improves exercise metabolism in patients with very long‐chain acyl‐CoA dehydrogenase deficiency

Author

Bleeker, Jeannette C., primary, Visser, Gepke, additional, Clarke, Kieran, additional, Ferdinandusse, Sacha, additional, de Haan, Ferdinand H., additional, Houtkooper, Riekelt H., additional, IJlst, Lodewijk, additional, Kok, Irene L., additional, Langeveld, Mirjam, additional, van der Pol, W. Ludo, additional, de Sain‐van der Velden, Monique G. M., additional, Sibeijn‐Kuiper, Anita, additional, Takken, Tim, additional, Wanders, Ronald J. A., additional, van Weeghel, Michel, additional, Wijburg, Frits A., additional, van der Woude, Luc H., additional, Wüst, Rob C. I., additional, Cox, Pete J., additional, and Jeneson, Jeroen A. L., additional

Published
2020
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39. Two Weeks of Smoking Cessation Reverse Cigarette Smoke-Induced Skeletal Muscle Atrophy and Mitochondrial Dysfunction in Mice

Author

Ajime, Tom Tanjeko, primary, Serré, Jef, additional, Wüst, Rob C I, additional, Messa, Guy Anselme Mpaka, additional, Poffé, Chiel, additional, Swaminathan, Anandini, additional, Maes, Karen, additional, Janssens, Wim, additional, Troosters, Thierry, additional, Degens, Hans, additional, and Gayan-Ramirez, Ghislaine, additional

Published
2020
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40. Altered mitochondrial metabolism in the insulin‐resistant heart

Author

Makrecka‐Kuka, Marina, primary, Liepinsh, Edgars, additional, Murray, Andrew J., additional, Lemieux, Hélène, additional, Dambrova, Maija, additional, Tepp, Kersti, additional, Puurand, Marju, additional, Käämbre, Tuuli, additional, Han, Woo H., additional, Goede, Paul, additional, O'Brien, Katie A., additional, Turan, Belma, additional, Tuncay, Erkan, additional, Olgar, Yusuf, additional, Rolo, Anabela P., additional, Palmeira, Carlos M., additional, Boardman, Neoma T., additional, Wüst, Rob C. I., additional, and Larsen, Terje S., additional

Published
2019
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44. Emerging Magnetic Resonance Imaging Techniques for Atherosclerosis Imaging

Author

Wüst, Rob C. I., Calcagno, Claudia, Daal, Mariah R. R., Nederveen, Aart J., Coolen, Bram F., Strijkers, Gustav J., Laboratory Genetic Metabolic Diseases, ACS - Diabetes & metabolism, ACS - Heart failure & arrhythmias, AMS - Ageing & Morbidty, Graduate School, ACS - Atherosclerosis & ischemic syndromes, AMS - Restoration & Development, AMS - Sports & Work, ANS - Brain Imaging, Radiology and Nuclear Medicine, Biomedical Engineering and Physics, CCA - Imaging and biomarkers, and AGEM - Amsterdam Gastroenterology Endocrinology Metabolism

Subjects
equipment and supplies, human activities
Abstract

Atherosclerosis is a prevalent disease affecting a large portion of the population at one point in their lives. There is an unmet need for noninvasive diagnostics to identify and characterize at-risk plaque phenotypes noninvasively and in vivo, to improve the stratification of patients with cardiovascular disease, and for treatment evaluation. Magnetic resonance imaging is uniquely positioned to address these diagnostic needs. However, currently available magnetic resonance imaging methods for vessel wall imaging lack sufficient discriminative and predictive power to guide the individual patient needs. To address this challenge, physicists are pushing the boundaries of magnetic resonance atherosclerosis imaging to increase image resolution, provide improved quantitative evaluation of plaque constituents, and obtain readouts of disease activity such as inflammation. Here, we review some of these important developments, with specific focus on emerging applications using high-field magnetic resonance imaging, the use of quantitative relaxation parameter mapping for improved plaque characterization, and novel 19F magnetic resonance imaging technology to image plaque inflammation.

Published
2019

45. Emerging Magnetic Resonance Imaging Techniques for Atherosclerosis Imaging: High Magnetic Field, Relaxation Time Mapping, and Fluorine-19 Imaging

Author

Wüst, Rob C I, Calcagno, Claudia, Daal, Mariah R R, Nederveen, Aart J, Coolen, Bram F, Strijkers, Gustav J, Wüst, Rob C I, Calcagno, Claudia, Daal, Mariah R R, Nederveen, Aart J, Coolen, Bram F, and Strijkers, Gustav J

Abstract

Atherosclerosis is a prevalent disease affecting a large portion of the population at one point in their lives. There is an unmet need for noninvasive diagnostics to identify and characterize at-risk plaque phenotypes noninvasively and in vivo, to improve the stratification of patients with cardiovascular disease, and for treatment evaluation. Magnetic resonance imaging is uniquely positioned to address these diagnostic needs. However, currently available magnetic resonance imaging methods for vessel wall imaging lack sufficient discriminative and predictive power to guide the individual patient needs. To address this challenge, physicists are pushing the boundaries of magnetic resonance atherosclerosis imaging to increase image resolution, provide improved quantitative evaluation of plaque constituents, and obtain readouts of disease activity such as inflammation. Here, we review some of these important developments, with specific focus on emerging applications using high-field magnetic resonance imaging, the use of quantitative relaxation parameter mapping for improved plaque characterization, and novel 19F magnetic resonance imaging technology to image plaque inflammation.

Published
2019
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47. Preclinical models versus clinical renal ischemia reperfusion injury: A systematic review based on metabolic signatures

Author

Lerink, Lente J. S., Kok, Michèle J. C., Mulvey, John F., Le Dévédec, Sylvia E., Markovski, Alexander A., Wüst, Rob C. I., Alwayn, Ian P. J., Ploeg, Rutger J., Schaapherder, Alexander F. M., Bakker, Jaap A., and Lindeman, Jan H. N.

Abstract

Despite decennia of research and numerous successful interventions in the preclinical setting, renal ischemia reperfusion (IR) injury remains a major problem in clinical practice, pointing toward a translational gap. Recently, two clinical studies on renal IR injury (manifested either as acute kidney injury or as delayed graft function) identified metabolic derailment as a key driver of renal IR injury. It was reasoned that these unambiguous metabolic findings enable direct alignment of clinical with preclinical data, thereby providing the opportunity to elaborate potential translational hurdles between preclinical research and the clinical context. A systematic review of studies that reported metabolic data in the context of renal IR was performed according to the PRISMA guidelines. The search (December 2020) identified 35 heterogeneous preclinical studies. The applied methodologies were compared, and metabolic outcomes were semi‐quantified and aligned with the clinical data. This review identifies profound methodological challenges, such as the definition of IR injury, the follow‐up time, and sampling techniques, as well as shortcomings in the reported metabolic information. In light of these findings, recommendations are provided in order to improve the translatability of preclinical models of renal IR injury. A comparison of metabolic responses in clinical and experimental renal ischemia reperfusion identifies multiple translational gaps.

Published
2022
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48. Commentaries on Viewpoint: The rigorous study of exercise adaptations: Why mRNA might not be enough

Author

Hornberger, Troy A., Carter, Heather N., Hood, David A., Figueiredo, Vandré Casagrande, Dupont-Versteegden, Esther E., Peterson, Charlotte A., McCarthy, John J., Camera, Donny M., Hawley, John A., Chaillou, Thomas, Cheng, Arthur J., Nader, Gustavo A., Wüst, Rob C. I., Houtkooper, Riekelt H., Other departments, Amsterdam Gastroenterology Endocrinology Metabolism, and Laboratory Genetic Metabolic Diseases

Subjects
0301 basic medicine, 03 medical and health sciences, 030104 developmental biology, Physiology, Physiology (medical), Integrative biology, Cellular level, Biology, Whole body, Neuroscience
Abstract

Integrative biology is needed to understand exercise adaptions from the whole body to the cellular level

Published
2016

49. Disturbed cardiac mitochondrial and cytosolic calcium handling in a metabolic risk‐related rat model of heart failure with preserved ejection fraction

Author

Miranda‐Silva, Daniela, primary, Wüst, Rob C. I., additional, Conceição, Glória, additional, Gonçalves‐Rodrigues, Patrícia, additional, Gonçalves, Nádia, additional, Gonçalves, Alexandre, additional, Kuster, Diederik W. D., additional, Leite‐Moreira, Adelino F., additional, Velden, Jolanda, additional, Sousa Beleza, Jorge M., additional, Magalhães, José, additional, Stienen, Ger J. M., additional, and Falcão‐Pires, Inês, additional

Published
2019
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50. Regular physical exercise mediates the immune response in atherosclerosis.

Author

do Brito Valente, André F., Jaspers, Richard T., and Wüst, Rob C. I.

Subjects
ATHEROSCLEROSIS, IMMUNE response, CARDIOVASCULAR diseases, ATHEROSCLEROTIC plaque, IMMUNOREGULATION
Abstract

Atherosclerosis is a chronic inflammatory cardiovascular disease, which results from lipid accumulation in the blood vessel wall, forming a plaque, and ultimately restricting blood flow. The immune system plays a vital role in progression to plaque rupture. While recent evidence clearly indicates the anti-inflammatory function of regular exercise, the mechanisms by which regular exercise can modulate its pathophysiology is not well understood. In this review, we discuss how regular exercise can lower systemic inflammation directly via modulation of the immune system or indirectly via altered myokine concentrations and metabolites. We describe the exercise-induced responses of various myokines (such as IL-6, adiponectin, and FGF21), and how cell function in the innate immune system can be modulated via regular exercise, with the aim to modulate plaque formation in atherosclerosis. [ABSTRACT FROM AUTHOR]

Published
2021

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