Fudi Wang

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: It is proposed that TRPML1 mediates a mechanism by which Fe2+ is released from late endosomes and lysosomes, and results indicate that impaired iron transport may contribute to both haematological and degenerative symptoms of ML4 patients.

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: The liver is identified as the primary organ that supports rapid erythrocyte removal and iron recycling, and a mechanism by which the body adapts to fluctuations in ery throatcyte integrity is uncovered.

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.