Luming Liu

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.

TL;DR: It is suggested that PBDE-47 disrupts mitochondrial dynamics to induce mitochondrial abnormalities, triggering apoptosis and thus contributing to neuronal loss and subsequent neurobehavioral deficits, and targeting mitochondrial fusion may be a promising therapeutic intervention against PBDEs neurotoxicity.

TL;DR: Autophagy impairment facilitates apoptosis, which, in turn, disrupts autophagy, ultimately resulting in cell death, and that Autophagy may act as a promising therapeutic target for PBDE-47-induced developmental neurotoxicity is suggested.

TL;DR: It is suggested that excessive ER stress, defective autophagy and the resultant apoptosis are implicated in maternal thyroid injury following perigestational PBDE-47 exposure, which offers insight into a better understanding of PBde-47-induced maternal thyroid toxicity.

TL;DR: It is suggested that perinatal low-dose PBDE-47 exposure hampers thyroglobulin turnover and induces thyroid cell apoptosis by triggering ER stress and lysosomal destabilization contributing to thyroid toxicity in adult female rats.