Baicalein protects cardiomyocytes from oxidative stress induced programmed necrosis by stabilizing carboxyl terminus of Hsc70-interacting protein.

Cardiomyocyte necrosis has been reported to be a major component in pathogenesis of cardiac diseases. We noticed that baicalein, a kind of principal components in the roots of Scutellaria baicalensis Georgi, exerts cardioprotective effects by inhibiting oxidative stress and apoptosis of Cardiomyocytes. However, it is rarely reported whether baicalein exerts myocardial protection by inhibiting necrosis.

miR-499-5p Attenuates Mitochondrial Fission and Cell Apoptosis via p21 in Doxorubicin Cardiotoxicity.

Doxorubicin (DOX) is a broad-spectrum anti-tumor drug, but its cardiotoxicity limits its clinical application. A better understanding of the molecular mechanisms underlying DOX cardiotoxicity will benefit clinical practice and remedy heart failure. Our present study observed that DOX caused cardiomyocyte (H9c2) apoptosis via the induction of abnormal mitochondrial fission.

ARC regulates programmed necrosis and myocardial ischemia/reperfusion injury through the inhibition of mPTP opening.

Necrosis is a key factor in myocardial injury during cardiac pathological processes, such as myocardial infarction (MI), ischemia/reperfusion (I/R) injury and heart failure. Increasing evidence suggests that several aspects of necrosis are programmed and tightly regulated, so targeting the necrosis process has become a new trend for myocardial protection. Multiple cellular signaling pathways have been implicated in necrotic cell death, such as the death receptor-mediated extrinsic and mitochondrial intrinsic pathways.

A polymorphism rs3746444 within the pre-miR-499 alters the maturation of miR-499-5p and its antiapoptotic function.

microRNAs (miRNAs) are non-coding RNAs that function as post-transcriptional regulators of cardiac development and cardiovascular diseases. Single nucleotide polymorphisms (SNPs) in miRNA genes are a novel class of genetic variations in the human genome that confer the risk of cardiovascular diseases. Here, we identified a polymorphism A→G (rs3746444) in miR-499 precursor (pre-miR-499) that affects the maturation of miR-499-5p and alters its antiapoptotic function by converting stable A-U base pair to wobble G-U base pair in pre-miR-499 secondary structure.

Molecular mechanism and therapy application of necrosis during myocardial injury.

Necrosis is an ancient topic which gains new attraction in the research area these years. There is no doubt that some necrosis can be regulated by genetic manipulation other than an accidental cell death resulting from physical or chemical stimuli. Recent advances in the molecular mechanism underlying the programmed necrosis show a fine regulation network which indicates new therapy targets in human diseases.