Polydatin post-treatment alleviates myocardial ischaemia/reperfusion injury by promoting autophagic flux

2016 ◽  
Vol 130 (18) ◽  
pp. 1641-1653 ◽  
Author(s):  
Yuanna Ling ◽  
Guiming Chen ◽  
Yi Deng ◽  
Huixiong Tang ◽  
Long Ling ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Reperfusion Injury ◽  
Myocardial Ischaemia ◽  
Reactive Oxygen ◽  
Post Treatment ◽  
Autophagic Flux ◽  
Oxygen Species ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion

The present paper provides evidence that polydatin (PD) post-treatment alleviates myocardial ischaemia/reperfusion (I/R) injury by promoting autophagic flux to clear damaged mitochondria to reduce reactive oxygen species (ROS) and cell death.

scholarly journals MCP-1 induces cardioprotection against ischaemia/reperfusion injury: role of reactive oxygen species

2008 ◽  
Vol 78 (3) ◽  
pp. 554-562 ◽  
Author(s):  
Hajime Morimoto ◽  
Masamichi Hirose ◽  
Masafumi Takahashi ◽  
Masanori Kawaguchi ◽  
Hirohiko Ise ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reperfusion Injury ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion

scholarly journals The role of mitochondrial reactive oxygen species, NO and H 2 S in ischaemia/reperfusion injury and cardioprotection

2020 ◽  
Vol 24 (12) ◽  
pp. 6510-6522 ◽  
Author(s):  
Ioanna Andreadou ◽  
Rainer Schulz ◽  
Andreas Papapetropoulos ◽  
Belma Turan ◽  
Kirsti Ytrehus ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reperfusion Injury ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Mitochondrial Reactive Oxygen Species ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion

scholarly journals Phospholipid oxidation products in ferroptotic myocardial cell death

2019 ◽  
Vol 317 (1) ◽  
pp. H156-H163 ◽  
Author(s):  
Aleksandra Stamenkovic ◽  
Grant N. Pierce ◽  
Amir Ravandi
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Myocardial Cell ◽  
Oxidation Products ◽  
Oxygen Species ◽  
New Therapeutic Approaches

Cell death is an important component of the pathophysiology of any disease. Myocardial disease is no exception. Understanding how and why cells die, particularly in the heart where cardiomyocyte regeneration is limited at best, becomes a critical area of study. Ferroptosis is a recently described form of nonapoptotic cell death. It is an iron-mediated form of cell death that occurs because of accumulation of lipid peroxidation products. Reactive oxygen species and iron-mediated phospholipid peroxidation is a hallmark of ferroptosis. To date, ferroptosis has been shown to be involved in cell death associated with Alzheimer’s disease, Huntington’s disease, cancer, Parkinson’s disease, and kidney degradation. Myocardial reperfusion injury is characterized by iron deposition as well as reactive oxygen species production. These conditions, therefore, favor the induction of ferroptosis. Currently there is no available treatment for reperfusion injury, which accounts for up to 50% of the final infarct size. This review will summarize the evidence that ferroptosis can induce cardiomyocyte death following reperfusion injury and the potential for this knowledge to open new therapeutic approaches for myocardial ischemia-reperfusion injury.

scholarly journals Activation of volume-sensitive Cl− channel mediates autophagy-related cell death in myocardial ischaemia/reperfusion injury

Oncotarget ◽  
2016 ◽  
Vol 7 (26) ◽  
pp. 39345-39362 ◽  
Author(s):  
Yuesheng Xia ◽  
Yan Liu ◽  
Tong Xia ◽  
Xing Li ◽  
Cong Huo ◽  
...  
Keyword(s):  
Cell Death ◽  
Reperfusion Injury ◽  
Myocardial Ischaemia ◽  
Ischaemia Reperfusion Injury ◽  
Cl Channel ◽  
Ischaemia Reperfusion ◽  
Related Cell

scholarly journals A study of free radical chemistry: their role and pathophysiological significance.

2013 ◽  
Vol 60 (1) ◽  
Author(s):  
Mariusz Gutowski ◽  
Sławomir Kowalczyk
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Redox Homeostasis ◽  
Reactive Oxygen ◽  
Oxygenic Photosynthesis ◽  
Oxygen Species ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion ◽  
Obstructive Sleep ◽  
Free Radical Chemistry

Oxygen is one of the most important molecules on Earth mainly because of the biochemical symmetry of oxygenic photosynthesis and aerobic respiration that can maintain homeostasis within our planet's biosphere. Oxygen can also produce toxic molecules, reactive oxygen species (ROS). ROS play a dual role in biological systems, since they can be either harmful or beneficial to living systems. They can be considered a double-edged sword because at moderate concentrations, nitric oxide (NO•), superoxide anion, and related reactive oxygen species play an important role as regulatory mediators in signalling processes. Many of the ROS-mediated responses actually protect the cells against oxidative stress and re-establish "redox homeostasis". On the other hand, overproduction of ROS has the potential to cause damage. In the recent decades, ROS has become a focus of interest in most biomedical disciplines and many types of clinical research. Increasing evidence from research on several diseases shows that oxidative stress is associated with the pathogenesis of diabetes mellitus, obesity, cancer, cardiovascular diseases, inflammation, ischaemia/reperfusion injury, obstructive sleep apnea, neurodegenerative disorders, hypertension and ageing.

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