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Conclusion PLB ameliorates DHT-induced mitochondrial dysfunction and ferroptosis in KGN cells by inhibiting YTHDF1 expression, and its action is dependent on the mechanism by which YTHDF1 regulates SLC7A5 translation through m6A modification
Eight-week swimming exercise pre-conditioning attenuates one-time exhaustion exercise-induced MQC deficits in the heart of obese mice, increases PINK1, SIRT1, PGC-1, Mfn1, and Drp1 protein expression, decreases p62 and Cyt-c protein levels, promotes mitophagy, mitochondrial biogenesis, and mitochondrial fission/fusion homeostasis, which in turn downregulates Bax protein expression, increases Bcl-2 and Bcl-2/BAX levels, and inhibits cardiac apoptosis in obese mice (Pires et al., 2022)
This also means the counteracted oxidative stress was as a result of the lysis of endothelial cells (Vukojevic et al., 2018)
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The up-regulated p53-serine15 phosphorylation (p53-pS15) in keloids is identified by phosphospecific protein microarray and western blotting
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