Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
Bugger, H; Pfeil, K.
Mitochondrial ROS in myocardial ischemia reperfusion and remodeling.
Biochim Biophys Acta Mol Basis Dis. 2020; 1866(7):165768-165768
Doi: 10.1016/j.bbadis.2020.165768
Web of Science
PubMed
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FullText_MUG
- Führende Autor*innen der Med Uni Graz
- Bugger Heiko Matthias
- Co-Autor*innen der Med Uni Graz
- Pfeil Katharina
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- Abstract:
- Despite major progress in interventional and medical treatments, myocardial infarction (MI) and subsequent development of heart failure (HF) are still associated with high mortality. Both during ischemia reperfusion (IR) in the acute setting of MI, as well as in the chronic remodeling process following MI, oxidative stress substantially contributes to cardiac damage. Reactive oxygen species (ROS) generated within mitochondria are particular drivers of mechanisms contributing to IR injury, including induction of mitochondrial permeability transition or oxidative damage of intramitochondrial structures and molecules. But even beyond the acute setting, mechanisms like inflammatory signaling, extracellular remodeling, or pro-apoptotic signaling that contribute to post-infarction remodeling are regulated by mitochondrial ROS. In the current review, we discuss both sources and consequences of mitochondrial ROS during IR and in the chronic setting following MI, thereby emphasizing the potential therapeutic value of attenuating mitochondrial ROS to improve outcome and prognosis for patients suffering MI. Copyright © 2020 Elsevier B.V. All rights reserved.
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- Mitochondria
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