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Increased mitochondrial fission and neuronal dysfunction in Huntingtons disease: implications for molecular inhibitors of excessive mitochondrial fission

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[DOI] [PMC free article] [PubMed] [Google Scholar] 126.Tomasi M.L., Ryoo M., Ramani K., Tomasi I., Giordano P., Mato J.M., Lu S.C., Lauda Tomasi M., Ryoo M., Ramani K., et al

[4] [6] In clinical contexts, high-dose intravenous ascorbic acid may modulate immune function, enhance wound healing, and support endothelial integrity

PINK1 stabilized by mitochondrial depolarization recruits Parkin to damaged mitochondria and activates latent Parkin for mitophagy

Also, mTORC1 activates the ribosomal protein S6 kinase beta-1 (S6K1) and the eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1), promoting the translation of MCL-1 mRNA on ribosomes and the synthesis of Mcl-1 [301]