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Pan Guo

Researcher at Third Military Medical University

Publications -  6
Citations -  757

Pan Guo is an academic researcher from Third Military Medical University. The author has contributed to research in topics: Melatonin & Mitochondrion. The author has an hindex of 6, co-authored 6 publications receiving 595 citations.

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Journal ArticleDOI

SIRT3-SOD2-mROS-dependent autophagy in cadmium-induced hepatotoxicity and salvage by melatonin

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.
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Dynamin 1-like-dependent mitochondrial fission initiates overactive mitophagy in the hepatotoxicity of cadmium.

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.
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Cadmium induced Drp1-dependent mitochondrial fragmentation by disturbing calcium homeostasis in its hepatotoxicity

TL;DR: Manipulation of Drp1 may be the potential avenue for developing novel strategies to protect against cadmium-induced hepatotoxicity as indicated by the effects and underlying mechanism of Cd on mitochondrial dynamics during hepatot toxicity.
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Melatonin prevents abnormal mitochondrial dynamics resulting from the neurotoxicity of cadmium by blocking calcium-dependent translocation of Drp1 to the mitochondria.

TL;DR: These results are the first to demonstrate that abnormal mitochondrial dynamics is involved in cadmium‐induced neurotoxicity and that Melatonin has significant pharmacological potential in protecting against the neurotoxicity of Cd by blocking the disbalance of mitochondrial fusion and fission.
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Melatonin Improves mitochondrial function by promoting MT1/SIRT1/PGC-1 alpha-dependent mitochondrial biogenesis in cadmium-induced hepatotoxicity in vitro.

TL;DR: SIRT1 plays an essential role in the ability of moderate melatonin to stimulate PGC-1 alpha and improve mitochondrial biogenesis and function at least partially through melatonin receptors in cadmium-induced hepatotoxicity, which indicates that Sirtinol and SIRT1 siRNA each blocked the melatonin-mediated elevation in mitochondrial function.