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Guoyu Zhou

Researcher at Huazhong University of Science and Technology

Publications -  32
Citations -  450

Guoyu Zhou is an academic researcher from Huazhong University of Science and Technology. The author has contributed to research in topics: Medicine & Chemistry. The author has an hindex of 10, co-authored 15 publications receiving 216 citations. Previous affiliations of Guoyu Zhou include Zhengzhou University.

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Excessive ER stress and the resulting autophagic flux dysfunction contribute to fluoride-induced neurotoxicity.

TL;DR: The in vivo results suggest that neuronal death resulted from excessive ER stress and autophagic flux dysfunction contributes to fluoride-elicited neurotoxicity.
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Thyroid function, intelligence, and low-moderate fluoride exposure among Chinese school-age children

TL;DR: Low-moderate fluoride exposure is associated with alterations in childhood thyroid function that may modify the association between fluoride and intelligence, and a significant modification effect by TSH was detected on the associations between urinary fluoride and IQ scores, without mediation by THs.
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SIRT1-dependent mitochondrial biogenesis supports therapeutic effects of resveratrol against neurodevelopment damage by fluoride.

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.
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Roles of mitochondrial fission inhibition in developmental fluoride neurotoxicity: mechanisms of action in vitro and associations with cognition in rats and children

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.
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Promotion of mitochondrial fusion protects against developmental PBDE-47 neurotoxicity by restoring mitochondrial homeostasis and suppressing excessive apoptosis.

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.