Junxia Min

TL;DR: It is discovered and demonstrated that ferroptosis, a programmed iron-dependent cell death, as a mechanism in murine models of doxorubicin (DOX)- and ischemia/reperfusion (I/R)-induced cardiomyopathy and Mitochondria-targeted antioxidant MitoTEMPO significantly rescued DOX cardiopathy, supporting oxidative damage of mitochondria as a major mechanism in ferroPTosis-induced heart damage.

TL;DR: Results provide compelling evidence that iron plays a key role in triggering Slc7a11‐mediated ferroPTosis and suggest that ferroptosis may be a promising target for treating hemochromatosis‐related tissue damage.

TL;DR: Findings provide compelling evidence that ferritin plays a major role in protecting against cardiac ferroptosis and subsequent heart failure, thereby providing a possible new therapeutic target for patients at risk of developing cardiomyopathy.

TL;DR: It is found that both acute cardiac injury and acute kidney injury are highly correlated with an increased risk of COVID-19-related mortality, and there is no correlation between chronic liver disease and increased disease severity.

TL;DR: Treating hepatocyte-specific Trf knockout mice with the ferroptosis inhibitor ferrostatin-1 potently rescued liver fibrosis induced by either high dietary iron or carbon tetrachloride (CCl4) injections, and deleting hepatic Slc39a14 expression in Trf-LKO mice significantly reduced hepatic iron accumulation, indicate that hepatic transferrin plays a protective role in maintaining liver function.