Jingwen Chen

TL;DR: The study suggests threshold and saturation effects of moderately excessive fluoride exposure on DF and intelligence loss in children, and a potential association between DF and the loss of excellent intelligence.

TL;DR: These findings provide deeper insights into roles of excessive apoptosis and defective autophagy in the aggravation of testicular damage, which could contribute to a better understanding of fluoride-induced male reproductive toxicity.

TL;DR: The in vivo results suggest that neuronal death resulted from excessive ER stress and autophagic flux dysfunction contributes to fluoride-elicited neurotoxicity.

TL;DR: In vivo and in vitro studies identified RSV, the strongest specific SIRT1 activator, improved mitochondrial biogenesis and subsequent mitochondrial function to protect against developmental fluoride neurotoxicity via activating SIRT2-dependent PGC-1α/NRF1/TFAM signaling pathway.

TL;DR: It is suggested that mitochondrial fission inhibition induces mitochondrial abnormalities, triggering abnormal autophagy and apoptosis, thus contributing to neuronal death, and that the mitochondrial dynamics molecules may act as promising indicators for developmental fluoride neurotoxicity.