Targeting mitochondrial shape: at the heart of cardioprotection
Authors (first, second and last of 10)
Collection
Mitochondria at the heart of cardioprotection
Acute myocardial infarction and the heart failure that often results remain the leading causes of death and disability worldwide. As such, new therapeutic targets need to be discovered to protect the myocardium against acute ischemia/reperfusion injury in order to reduce myocardial infarct size, preserve left ventricular function and prevent the onset of heart failure. Mitochondrial dysfunction during acute ischemia/reperfusion injury is a critical determinant of cell death following acute myocardial infarction and therefore, ion channels in the inner mitochondrial membrane, which are known to influence cell death and survival, provide potential therapeutic targets for cardioprotection. Even more, several interventions, such as ischemic conditioning strategies are known to decrease lethal myocardial ischemia/reperfusion injury and they all have a common end point, namely, the mitochondria. Therefore, in the present themed issue of Basic Research in Cardiology, the role of mitochondria in cardioprotection with focus om alterations of mitochondrial function, formation of reactive oxygen species, opening of the mitochondrial permeability transition pore, kinase signalling and mitochondrial dynamics are discussed.
Editors
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Rainer Schulz
Professor Rainer Schulz is Head of the Institute of Physiology at the Justus-Liebig University (JLU) in Giessen, Germany. His research is related to ischemia/reperfusion injury and protection from it, especially on the cross talk between protein kinases and mitochondrial proteins (namely connexin 43, p66shc and monoamine oxidases) involved in cardioprotection. More recently, as part of the cardiopulmonary institute (CPI) of the JLU and PI of the CRC1213 of the German Research Foundation, his research has expanded to the pulmonary circulation and pulmonary hypertension.
Articles (9 in this collection)
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Authors (first, second and last of 18)
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Deficiency of mitochondrial calcium uniporter abrogates iron overload-induced cardiac dysfunction by reducing ferroptosis
Authors (first, second and last of 12)
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SMYD1a protects the heart from ischemic injury by regulating OPA1-mediated cristae remodeling and supercomplex formation
Authors (first, second and last of 24)
