Cardiovascular diseases (CVDs), such as ischaemic heart disease, cardiomyopathy,
atherosclerosis, hypertension, stroke and heart failure, are among the leading causes of …

Myocardial infarction (MI) is the irreversible death of cardiomyocyte secondary to prolonged
lack of oxygen or fresh blood supply. Historically considered as merely cardiomyocyte …

Mitophagy preserves microvascular structure and function during myocardial
ischemia/reperfusion (I/R) injury. Empagliflozin, an anti-diabetes drug, may also protect …

Abstract Necrostatin-1 (Nec-1) is a RIP1-targeted inhibitor of necroptosis, a form of
programmed cell death discovered and investigated in recent years. There are already …

Mitochondrial damage is a critical contributor to cardiac ischemia/reperfusion (I/R) injury.
Mitochondrial quality control (MQC) mechanisms, a series of adaptive responses that …

Increased mitochondrial damage is related to the progression of a diet-induced nonalcoholic
fatty liver disease. The aim of our study is to investigate the role of Sirtuin 3 (Sirt3) in treating …

The death of cardiomyocytes either through apoptosis or necroptosis is the pathological
feature of cardiac ischemia-reperfusion (I/R) injury. Phosphoglycerate mutase 5 (PGAM5), a …

Myocardial infarction (MI) is a leading cause of morbidity and mortality worldwide. As
mitochondrial dysfunction critically contributes to the pathogenesis of MI, intensive research …

Despite significant advances in the treatment of myocardial ischemia-reperfusion (I/R) injury,
coronary circulation is a so far neglected target of cardioprotection. In this study, we …

Ferroptosis is a nonapoptotic form of cell death characterized by iron‐dependent
accumulation of lipid hydroperoxides to lethal levels. Necroptosis, an alternative form of …