Yonghui Lu

TL;DR: Melatonin exerts a hepatoprotective effect on mitochondrial-derived O2•−-stimulated autophagic cell death that is dependent on the SIRT3/SOD2 pathway, and is reported to protect against Cd-induced hepatotoxicity.

TL;DR: The results suggest that melatonin confers protection against Cd‐induced liver inflammation and hepatocyte death via inhibition of the TXNIP‐NLRP3 inflammasome pathway.

TL;DR: The results suggest that ER signaling-mediated meiotic disruption may be a major contributor to the molecular events leading to BPA-related male reproductive disorders, and support the growing association between BPA exposure and the rapid increase in the incidence ofmale reproductive disorders.

TL;DR: The data suggest that NLRP3 inflammasome, activated by the generation of mtROS, mediates Cd-induced pyroptosis in HUVECs, and provides novel insights into C d-induced cytotoxicity and the underlying mechanism by which Cd induces endothelial injury.

TL;DR: It is indicated that Cd induces mitochondrial loss via the overactivation of mitophagy following DNM1L-dependent mitochondrial fragmentation, and the balanced activity of D NM1L and mitophile signaling may be a potential therapeutic approach to treat Cd-induced hepatotoxicity.