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1. Positioning of nucleosomes containing γ-H2AX precedes active DNA demethylation and transcription initiation

Author

Dobersch, Stephanie, Rubio, Karla, Singh, Indrabahadur, Günther, Stefan, Graumann, Johannes, Cordero, Julio, Castillo-Negrete, Rafael, Huynh, Minh Bao, Mehta, Aditi, Braubach, Peter, Cabrera-Fuentes, Hector, Bernhagen, Jürgen, Chao, Cho-Ming, Bellusci, Saverio, Günther, Andreas, Preissner, Klaus T., Kugel, Sita, Dobreva, Gergana, Wygrecka, Malgorzata, Braun, Thomas, Papy-Garcia, Dulce, and Barreto, Guillermo

Published
2021
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4. FURIN Inhibition Reduces Vascular Remodeling and Atherosclerotic Lesion Progression in Mice

Author

Yakala, Gopala K., Cabrera-Fuentes, Hector A., Crespo-Avilan, Gustavo E., Rattanasopa, Chutima, Burlacu, Alexandrina, George, Benjamin L., Anand, Kaviya, Mayan, David Castaño, Corlianò, Maria, Hernández-Reséndiz, Sauri, Wu, Zihao, Schwerk, Anne M.K., Tan, Amberlyn L.J., Trigueros-Motos, Laia, Chèvre, Raphael, Chua, Tricia, Kleemann, Robert, Liehn, Elisa A., Hausenloy, Derek J., Ghosh, Sujoy, and Singaraja, Roshni R.

Published
2019
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5. Inactivation of nuclear histone deacetylases by EP300 disrupts the MiCEE complex in idiopathic pulmonary fibrosis

Author

Rubio, Karla, Singh, Indrabahadur, Dobersch, Stephanie, Sarvari, Pouya, Günther, Stefan, Cordero, Julio, Mehta, Aditi, Wujak, Lukasz, Cabrera-Fuentes, Hector, Chao, Cho-Ming, Braubach, Peter, Bellusci, Saverio, Seeger, Werner, Günther, Andreas, Preissner, Klaus T., Wygrecka, Malgorzata, Savai, Rajkumar, Papy-Garcia, Dulce, Dobreva, Gergana, Heikenwalder, Mathias, Savai-Pullamsetti, Soni, Braun, Thomas, and Barreto, Guillermo

Published
2019
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6. Remote ischemic preconditioning in patients undergoing cardiac surgery with six ischemic cycles.

Author

Böning, Andreas, Flicker, Luisa, Rodriguez-Montesinos, Julian, Cabrera-Fuentes, Hector, Preissner, Klaus T, Niemann, Bernd, and Taghiyev, Zulfugar T

Subjects
RNA physiology, CARDIAC surgery, STATISTICS, NONPARAMETRIC statistics, MYOCARDIUM, ISCHEMIC preconditioning, ANALYSIS of variance, CONFIDENCE intervals, MYOCARDIAL ischemia, SURGERY, PATIENTS, BLOOD collection, RNA, MANN Whitney U Test, FISHER exact test, CELLULAR signal transduction, TREATMENT effectiveness, MYOCARDIAL reperfusion complications, T-test (Statistics), TUMOR necrosis factors, REPEATED measures design, STATISTICAL hypothesis testing, DESCRIPTIVE statistics, EXTRACELLULAR space, DATA analysis, DATA analysis software
Abstract

Background: We have previously shown that remote ischemic preconditioning (RIP), which utilizes in part the extracellular RNA (eRNA)/RNase1 pathway, can induce ischemic tolerance in humans. Because RIP has thus far been tested only with four cycles of extremity ischemia/reperfusion, we investigated the influence of six cycles of ischemia on the eRNA/RNase1 pathway in cardiac patients. Methods: Six cycles of RIP were carried out in 14 patients undergoing cardiac surgery. Blood samples were taken at 13 timepoints during surgery and at three timepoints after surgery for determining serum levels of RNase1, eRNA, and TNF-α. Trans-cardiac gradients between the myocardial blood inflow and outflow were calculated. Results: Between the fourth and the sixth RIP cycles, a noticeable increase in the levels of eRNA (fourth: 151.6 (SD: 44.2) ng/ml vs sixth: 181.8 (SD: 87.5) ng/ml, p =.071), and a significant increase in RNase1 (fourth: 151.1 (SD: 42.6) U/ml vs sixth: 175.3 (SD: 41.2) U/ml, p =.001), were noted. The trans-cardiac gradients of RNase1 and eRNA before and after ischemia were not significantly different (p =.158 and p =.221; p =.397 and p =.683, respectively). Likewise, the trans-cardiac gradient of TNF-α was similar before and after ischemia. During the first 48 h after the surgery, RNase1 activity rose significantly and exceeded baseline values (135.7 (SD: 40.6) U/ml before and 279.2 (SD: 85.6) U/ml after surgery, p =.001) as did eRNA levels (148,6 (SD: 35.4) ng/ml before and 396.5 (SD: 154.5) ng/ml after surgery, p =.005), whereas TNF-α levels decreased significantly (91.7 (SD: 47.7) pg/ml before and 35.7 (SD: 36.9) pg/ml after surgery, p =.001). Conclusion: Six RIP cycles increased the RNase1 levels significantly above those observed with four cycles. More clinical data are required to show whether this translates into a benefit for patients. [ABSTRACT FROM AUTHOR]

Published
2023
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12. From basic mechanisms to clinical applications in heart protection, new players in cardiovascular diseases and cardiac theranostics: meeting report from the third international symposium on “New frontiers in cardiovascular research”

Author

Cabrera-Fuentes, Hector A., Aragones, Julian, Bernhagen, Jürgen, Boening, Andreas, Boisvert, William A., Bøtker, Hans E., Bulluck, Heerajnarain, Cook, Stuart, Di Lisa, Fabio, Engel, Felix B., Engelmann, Bernd, Ferrazzi, Fulvia, Ferdinandy, Péter, Fong, Alan, Fleming, Ingrid, Gnaiger, Erich, Hernández-Reséndiz, Sauri, Kalkhoran, Siavash Beikoghli, Kim, Moo Hyun, Lecour, Sandrine, Liehn, Elisa A., Marber, Michael S., Mayr, Manuel, Miura, Tetsuji, Ong, Sang-Bing, Peter, Karlheinz, Sedding, Daniel, Singh, Manvendra K., Suleiman, M. Saadeh, Schnittler, Hans J., Schulz, Rainer, Shim, Winston, Tello, Daniel, Vogel, Carl-Wilhelm, Walker, Malcolm, Li, Qilong Oscar Yang, Yellon, Derek M., Hausenloy, Derek J., and Preissner, Klaus T.

Published
2016
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14. Meeting report from the 2nd International Symposium on New Frontiers in Cardiovascular Research. Protecting the cardiovascular system from ischemia: between bench and bedside

Author

Cabrera-Fuentes, Hector A., Alba-Alba, Corina, Aragones, Julian, Bernhagen, Jürgen, Boisvert, William A., Bøtker, Hans E., Cesarman-Maus, Gabriela, Fleming, Ingrid, Garcia-Dorado, David, Lecour, Sandrine, Liehn, Elisa, Marber, Michael S., Marina, Nephtali, Mayr, Manuel, Perez-Mendez, Oscar, Miura, Tetsuji, Ruiz-Meana, Marisol, Salinas-Estefanon, Eduardo M., Ong, Sang-Bing, Schnittler, Hans J., Sanchez-Vega, Jose T., Sumoza-Toledo, Adriana, Vogel, Carl-Wilhelm, Yarullina, Dina, Yellon, Derek M., Preissner, Klaus T., and Hausenloy, Derek J.

Published
2015
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16. Nanoparticle delivery of cardioprotective therapies

Author

Mendez-Fernandez, Abraham, Cabrera-Fuentes, Hector A, Velmurugan, Bhaarathy, Irei, Jason, Boisvert, William A., Lu, Shengjie, and Hausenloy, Derek J

Subjects
cardiovascular diseases, Article
Abstract

Acute myocardial infarction (AMI), and the heart failure (HF) that often follows, are leading causes of death and disability worldwide. Crucially, there are currently no effective treatments, other than myocardial reperfusion, for reducing myocardial infarct (MI) size and preventing HF following AMI. Thus, there is an unmet need to discover novel cardioprotective therapies to reduce MI size, and prevent HF in AMI patients. Although a large number of therapies have been shown to reduce MI size in experimental studies, the majority have failed to benefit AMI patients. Failure to deliver cardioprotective therapy to the ischemic heart in sufficient concentrations following AMI is a major factor for the lack of success observed in previous clinical cardioprotection studies. Therefore, new strategies are needed to improve the delivery of cardioprotective therapies to the ischemic heart following AMI. In this regard, nanoparticles have emerged as drug delivery systems for improving the bioavailability, delivery, and release of cardioprotective therapies, and should result in improved efficacy in terms of reducing MI size and preventing HF. In this article, we provide a review of currently available nanoparticles, some of which have been FDA-approved, in terms of their use as drug delivery systems in cardiovascular disease and cardioprotection.

Published
2020

17. Mitochondrial and mitochondrial‐independent pathways of myocardial cell death during ischaemia and reperfusion injury

Author

Davidson, Sean M; https://orcid.org/0000-0001-5182-4980, Adameová, Adriana, Barile, Lucio, Cabrera‐Fuentes, Hector Alejandro; https://orcid.org/0000-0002-8502-7098, Lazou, Antigone; https://orcid.org/0000-0002-7889-9648, Pagliaro, Pasquale, Stensløkken, Kåre‐Olav, Garcia‐Dorado, David, Davidson, Sean M; https://orcid.org/0000-0001-5182-4980, Adameová, Adriana, Barile, Lucio, Cabrera‐Fuentes, Hector Alejandro; https://orcid.org/0000-0002-8502-7098, Lazou, Antigone; https://orcid.org/0000-0002-7889-9648, Pagliaro, Pasquale, Stensløkken, Kåre‐Olav, and Garcia‐Dorado, David

Abstract

Acute myocardial infarction causes lethal injury to cardiomyocytes during both ischaemia and reperfusion (IR). It is important to define the precise mechanisms by which they die in order to develop strategies to protect the heart from IR injury. Necrosis is known to play a major role in myocardial IR injury. There is also evidence for significant myocardial death by other pathways such as apoptosis, although this has been challenged. Mitochondria play a central role in both of these pathways of cell death, as either a causal mechanism is the case of mitochondrial permeability transition leading to necrosis, or as part of the signalling pathway in mitochondrial cytochrome c release and apoptosis. Autophagy may impact this process by removing dysfunctional proteins or even entire mitochondria through a process called mitophagy. More recently, roles for other programmed mechanisms of cell death such as necroptosis and pyroptosis have been described, and inhibitors of these pathways have been shown to be cardioprotective. In this review, we discuss both mitochondrial and mitochondrial‐independent pathways of the major modes of cell death, their role in IR injury and their potential to be targeted as part of a cardioprotective strategy. This article is part of a special Issue entitled ‘Mitochondria as targets of acute cardioprotection’ and emerged as part of the discussions of the European Union (EU)‐CARDIOPROTECTION Cooperation in Science and Technology (COST) Action, CA16225.

Published
2020

21. Positioning of nucleosomes containing γ-H2AX precedes active DNA demethylation and transcription initiation

Author

Dobersch, Stephanie, primary, Rubio, Karla, additional, Singh, Indrabahadur, additional, Günther, Stefan, additional, Graumann, Johannes, additional, Cordero, Julio, additional, Castillo-Negrete, Rafael, additional, Huynh, Minh Bao, additional, Mehta, Aditi, additional, Braubach, Peter, additional, Cabrera-Fuentes, Hector, additional, Bernhagen, Jürgen, additional, Chao, Cho-Ming, additional, Bellusci, Saverio, additional, Günther, Andreas, additional, Preissner, Klaus T, additional, Dobreva, Gergana, additional, Wygrecka, Malgorzata, additional, Braun, Thomas, additional, Papy-Garcia, Dulce, additional, and Barreto, Guillermo, additional

Published
2020
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24. Circulating blood cells and extracellular vesicles in acute cardioprotection

Author

Davidson, Sean M, Andreadou, Ioanna, Barile, Lucio, Birnbaum, Yochai, Cabrera-Fuentes, Hector A, Cohen, Michael V, Downey, James M, Girao, Henrique, Pagliaro, Pasquale, Penna, Claudia, Pernow, John, Preissner, Klaus T, Ferdinandy, Peter, Davidson, Sean M, Andreadou, Ioanna, Barile, Lucio, Birnbaum, Yochai, Cabrera-Fuentes, Hector A, Cohen, Michael V, Downey, James M, Girao, Henrique, Pagliaro, Pasquale, Penna, Claudia, Pernow, John, Preissner, Klaus T, and Ferdinandy, Peter

Abstract

During an ST-elevation myocardial infarction (STEMI), the myocardium undergoes a prolonged period of ischaemia. Reperfusion therapy is essential to minimize cardiac injury but can paradoxically cause further damage. Experimental procedures to limit ischaemia and reperfusion (IR) injury have tended to focus on the cardiomyocytes since they are crucial for cardiac function. However, there is increasing evidence that non-cardiomyocyte resident cells in the heart (as discussed in a separate review in this Spotlight series) as well as circulating cells and factors play important roles in this pathology. For example, erythrocytes, in addition to their main oxygen-ferrying role, can protect the heart from IR injury via the export of nitric oxide bioactivity. Platelets are well-known to be involved in haemostasis and thrombosis, but beyond these roles, they secrete numerous factors including sphingosine-1 phosphate (S1P), platelet activating factor (PAF) and cytokines that can all strongly influence the development of IR injury. This is particularly relevant given that most STEMI patients receive at least one type of platelet inhibitor. Moreover, there are large numbers of circulating vesicles in the blood, including microvesicles and exosomes, which can exert both beneficial and detrimental effects on IR injury. Some of these effects are mediated by the transfer of miRNA to the heart. Synthetic miRNA molecules may offer an alternative approach to limiting the response to IR injury. We discuss these and other circulating factors, focussing on potential therapeutic targets relevant to IR injury. Given the prevalence of co-morbidities such as diabetes in the target patient population, their influence will also be discussed. This article is part of a Cardiovascular Research Spotlight Issue entitled 'Cardioprotection Beyond the Cardiomyocyte', and emerged as part of the discussions of the European Union (EU)-CARDIOPROTECTION Cooperation in Science and Technology (COST) Action

Published
2019

26. The Role of Platelets in Ischemic Conditioning

Author

Alpuche, Juan, Quírino, Luz, Sánchez-Vega, José T, Yap, Jonathan, Pérez-Campos, Eduardo, and Cabrera-Fuentes, Hector A.

Subjects
cardiovascular diseases, Article
Abstract

Ischemic heart disease (IHD) is one of the leading causes of death and disability worldwide. Platelets, as the main regulators of hemostasis, are major players in acute myocardial ischemia/reperfusion injury (IRI). Additionally, platelets are modified by endogenous cardioprotective strategies such as ischemic preconditioning, postconditioning, and remote ischemic conditioning. In this article, we provide an overview of the functionional role of platelets in acute myocardial IRI, and highlight their potential as targets for cardioprotection to improve health outcomes in patients with IHD.

Published
2018

27. Targeting Mitochondrial Fission Using Mdivi-1 in A Clinically Relevant Large Animal Model of Acute Myocardial Infarction: A Pilot Study

Author

Ong, Sang-Bing, primary, Kwek, Xiu-Yi, additional, Katwadi, Khairunnisa, additional, Hernandez-Resendiz, Sauri, additional, Crespo-Avilan, Gustavo, additional, Ismail, Nur, additional, Lin, Ying-Hsi, additional, Yap, En, additional, Lim, Song-Yi, additional, Ja, K, additional, Ramachandra, Chrishan, additional, Tee, Nicole, additional, Toh, Jin, additional, Shim, Winston, additional, Wong, Philip, additional, Cabrera-Fuentes, Hector, additional, and Hausenloy, Derek, additional

Published
2019
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30. Circulating blood cells and extracellular vesicles in acute cardioprotection

Author

Davidson, Sean M, primary, Andreadou, Ioanna, additional, Barile, Lucio, additional, Birnbaum, Yochai, additional, Cabrera-Fuentes, Hector A, additional, Cohen, Michael V, additional, Downey, James M, additional, Girao, Henrique, additional, Pagliaro, Pasquale, additional, Penna, Claudia, additional, Pernow, John, additional, Preissner, Klaus T, additional, and Ferdinandy, Péter, additional

Published
2018
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31. Innate immunity as a target for acute cardioprotection

Author

Zuurbier, Coert J, primary, Abbate, Antonio, additional, Cabrera-Fuentes, Hector A, additional, Cohen, Michael V, additional, Collino, Massimo, additional, De Kleijn, Dominique P V, additional, Downey, James M, additional, Pagliaro, Pasquale, additional, Preissner, Klaus T, additional, Takahashi, Masafumi, additional, and Davidson, Sean M, additional

Published
2018
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33. Circadian variation in acute myocardial infarct size assessed by cardiovascular magnetic resonance in reperfused STEMI patients

Author

Bulluck, Heerajnarain, Nicholas, Jennifer, Crimi, Gabriele, White, Steven K, Ludman, Andrew J, Pica, Silvia, Raineri, Claudia, Cabrera-Fuentes, Hector A, Yellon, Derek, Rodriguez-Palomares, Jose, Garcia-Dorado, David, and Hausenloy, Derek J

Subjects
ST-segment elevation myocardial infarction, Myocardial infarct size, Circadian rhythm, Cardiovascular magnetic resonance, cardiovascular diseases, Cardiology and Cardiovascular Medicine, Article
Abstract

Objective Clinical studies using serum cardiac biomarkers to investigate a circadian variation in acute myocardial infarct (MI) size in ST-segment elevation myocardial infarction (STEMI) patients reperfused by primary percutaneous coronary intervention (PPCI) have produced mixed results. We aimed to investigate this phenomenon using acute MI size measured by cardiovascular magnetic resonance (CMR). Methods Patient-level data was obtained from 4 randomized controlled trials investigating the MI-limiting effects of cardioprotective therapies in this pooled analysis. The primary analysis was performed in those patients with no pre-infarct angina; duration of ischemia > 60 min and

Published
2016

35. Mitochondrial and mitochondrial‐independent pathways of myocardial cell death during ischaemia and reperfusion injury.

Author

Davidson, Sean M., Adameová, Adriana, Barile, Lucio, Cabrera‐Fuentes, Hector Alejandro, Lazou, Antigone, Pagliaro, Pasquale, Stensløkken, Kåre‐Olav, and Garcia‐Dorado, David

Subjects
CELL death, APOPTOSIS, REPERFUSION injury, NECROSIS, CYTOCHROME c, MYOCARDIAL infarction
Abstract

Acute myocardial infarction causes lethal injury to cardiomyocytes during both ischaemia and reperfusion (IR). It is important to define the precise mechanisms by which they die in order to develop strategies to protect the heart from IR injury. Necrosis is known to play a major role in myocardial IR injury. There is also evidence for significant myocardial death by other pathways such as apoptosis, although this has been challenged. Mitochondria play a central role in both of these pathways of cell death, as either a causal mechanism is the case of mitochondrial permeability transition leading to necrosis, or as part of the signalling pathway in mitochondrial cytochrome c release and apoptosis. Autophagy may impact this process by removing dysfunctional proteins or even entire mitochondria through a process called mitophagy. More recently, roles for other programmed mechanisms of cell death such as necroptosis and pyroptosis have been described, and inhibitors of these pathways have been shown to be cardioprotective. In this review, we discuss both mitochondrial and mitochondrial‐independent pathways of the major modes of cell death, their role in IR injury and their potential to be targeted as part of a cardioprotective strategy. This article is part of a special Issue entitled 'Mitochondria as targets of acute cardioprotection' and emerged as part of the discussions of the European Union (EU)‐CARDIOPROTECTION Cooperation in Science and Technology (COST) Action, CA16225. [ABSTRACT FROM AUTHOR]

Published
2020
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36. Diagnosis of Transient/Latent HPV Infections - A Point of View!

Author

Perez-Campos Mayoral, Eduardo, primary, Mayoral-Andrade, Gabriel, additional, Pérez-Campos Mayoral, Laura, additional, Canseco, Socorro Pina, additional, Cruz, Ruth Martínez, additional, Hernández-Huerta, María Teresa, additional, Rodriguez, Adriana Moreno, additional, Cabrera-Fuentes, Hector A., additional, and Pérez-Campos, Eduardo, additional

Published
2018
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39. Targeting of Extracellular RNA Reduces Edema Formation and Infarct Size and Improves Survival After Myocardial Infarction in Mice

Author

Stieger, Philipp, primary, Daniel, Jan‐Marcus, additional, Thölen, Christiane, additional, Dutzmann, Jochen, additional, Knöpp, Kai, additional, Gündüz, Dursun, additional, Aslam, Muhammad, additional, Kampschulte, Marian, additional, Langheinrich, Alexander, additional, Fischer, Silvia, additional, Cabrera‐Fuentes, Hector, additional, Wang, Yong, additional, Wollert, Kai C., additional, Bauersachs, Johann, additional, Braun‐Dullaeus, Rüdiger, additional, Preissner, Klaus T., additional, and Sedding, Daniel G., additional

Published
2017
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40. HMGA2 mediated epigenetic regulation of Gata6 controls epithelial WNT signaling during lung development

Author

Singh, Indrabahadur, primary, Mehta, Aditi, additional, Öztürk, Nihan, additional, Cordero, Julio, additional, Contreras, Adriana, additional, Hasan, Diya, additional, Cosentino, Claudia, additional, Sebastian, Carlos, additional, Krüger, Marcus, additional, Looso, Mario, additional, Boettger, Thomas, additional, Cabrera-Fuentes, Hector A, additional, Carraro, Gianni, additional, Wheeler, Matthew, additional, Bellusci, Saverio, additional, Mostoslavsky, Raul, additional, Seeger, Werner, additional, Braun, Thomas, additional, and Barreto, Guillermo, additional

Published
2017
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41. Assessing the effects of mitofusin 2 deficiency in the adult heart using 3D electron tomography

Author

Beikoghli Kalkhoran, Siavash, primary, Hall, Andrew R., additional, White, Ian J., additional, Cooper, Jackie, additional, Fan, Qiao, additional, Ong, Sang-Bing, additional, Hernández-Reséndiz, Sauri, additional, Cabrera-Fuentes, Hector, additional, Chinda, Kroekkiat, additional, Chakraborty, Bibhas, additional, Dorn, Gerald W., additional, Yellon, Derek M., additional, and Hausenloy, Derek J., additional

Published
2017
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42. Full left ventricular coverage is essential for the accurate quantification of the area-at-risk by T1 and T2 mapping

Author

Bulluck, Heerajnarain, primary, Bryant, Jennifer A., additional, Lim, Mei Xing, additional, Tan, Xiao Wei, additional, Ramlall, Manish, additional, Francis, Rohin, additional, Kotecha, Tushar, additional, Cabrera-Fuentes, Hector A., additional, Knight, Daniel S., additional, Fontana, Marianna, additional, Moon, James C., additional, and Hausenloy, Derek J., additional

Published
2017
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43. Quantifying the area-at-risk of myocardial infarction in-vivo using arterial spin labeling cardiac magnetic resonance

Author

Dongworth, Rachel K., primary, Campbell-Washburn, Adrienne E., additional, Cabrera-Fuentes, Hector A., additional, Bulluck, Heerajnarain, additional, Roberts, Thomas, additional, Price, Anthony N., additional, Hernández-Reséndiz, Sauri, additional, Ordidge, Roger J., additional, Thomas, David L., additional, Yellon, Derek M., additional, Lythgoe, Mark F., additional, and Hausenloy, Derek J., additional

Published
2017
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44. Reply to “Circadian variation in acute myocardial infarction size: Likely involvement of the melatonin and suprachiasmatic nuclei”

Author

Bulluck, Heerajnarain, primary, Nicholas, Jennifer, additional, Crimi, Gabriele, additional, White, Steven K, additional, Ludman, Andrew J, additional, Pica, Silvia, additional, Raineri, Claudia, additional, Cabrera-Fuentes, Hector A, additional, Yellon, Derek M, additional, Rodriguez-Palomares, Jose, additional, Garcia-Dorado, David, additional, and Hausenloy, Derek J, additional

Published
2017
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45. Platelets and Platelet-Derived Microvesicles as Immune Effectors in Type 2 Diabetes

Author

Cortez-Espinosa, Nancy, primary, Perez-Campos Mayoral, Laura, additional, Perez-Campos, Eduardo, additional, Alejandro Cabrera Fuentes, Hector, additional, Perez-Campos Mayoral, Eduardo, additional, Martínez-Cruz, Ruth, additional, Pina Canseco, Socorro, additional, Mayoral Andrade, Gabriel, additional, Martinez Cruz, Margarito, additional, Gallegos Velasco, Itandehui, additional, and Hernandez Cruz, Pedro, additional

Published
2017
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47. Reply

Author

Bulluck, Heerajnarain, primary, Foin, Nicolas, additional, Cabrera-Fuentes, Hector A., additional, Yeo, Khung K., additional, Wong, Aaron S., additional, Fam, Jiang M., additional, Wong, Philip E., additional, Tan, Jack W., additional, Low, Adrian F., additional, and Hausenloy, Derek J., additional

Published
2017
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48. Correction: Influence of Extracellular RNAs, Released by Rheumatoid Arthritis Synovial Fibroblasts, on Their Adhesive and Invasive Properties

Author

Zimmermann-Geller, Birgit, primary, Köppert, Sina, additional, Fischer, Silvia, additional, Cabrera-Fuentes, Hector A., additional, Lefèvre, Stephanie, additional, Rickert, Markus, additional, Steinmeyer, Jürgen, additional, Rehart, Stefan, additional, Umscheid, Thomas, additional, Schönburg, Markus, additional, Müller-Ladner, Ulf, additional, Preissner, Klaus T., additional, Frommer, Klaus W., additional, and Neumann, Elena, additional

Published
2017
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