SIRT1, SIRT3 and SIRT6 act as core cardioprotective subtypes: they synergistically activate the AMPK/Nrf2 antioxidant axis to block reperfusion oxidative injury and form an integrated endogenous protective network targeting all core pathological links of MIRI.
Myocardial ischemia–reperfusion injury (MIRI) is a critical pathological paradox following revascularization in acute myocardial infarction, yet effective clinical interventions remain limited. MIRI involves a complex, interlinked hierarchy of programmed cell death modalities, including ferroptosis, pyroptosis, and cup...
Dong Zhang, Xiao-Ting Yang, Sheng-Yu Gong et al.· Reviews in cardiovascular me...· 0 citations
Myocardial ischemia–reperfusion (I/R) injury remains a major limitation in cardiovascular therapy, where restoration of blood flow paradoxically initiates oxidative stress, inflammation, mitochondrial dysfunction, and cardiomyocyte death. Although multiple pharmacological strategies have been investigated, clinical tra...
R. A. Syahputra, Princella Halim, Sasniwiati Sari Hasibuan et al.· Journal of biochemical and m...· 0 citations
Acute myocardial infarction (AMI) remains the leading cause of cardiovascular death and disability worldwide. With the advances in percutaneous coronary intervention and coronary artery bypass grafting, timely revascularization has become the main approach to limit infarct size and improve heart function and prognosis....
Shen-Shen Ding, Xiao-Ding Zhang, Zu-Xian Sheng et al.· Frontiers in Cell and Develo...· 0 citations
Myocardial ischemia–reperfusion injury (MIRI) is driven by dynamic metabolic disturbances that extend beyond adenosine triphosphate depletion and encompass mitochondrial dysfunction, redox imbalance, calcium overload, iron dysregulation, lipid peroxidation, and inflammatory activation. These alterations regulate multip...