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Description

This mitochondrial dysfunction-induced immunosenescence promotes premature aging phenotypes and multimorbidity, creating a pro-inflammatory environment that simultaneously accelerates atherosclerosis progression and neuroinflammation

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Intriguingly, when these enzymes bind with zinc, the oxidation of cysteine residues is inhibited, temporarily reviving their enzymatic activity (Mnico et al

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Excess collagen production may also cause keloid scars to form

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Teperek, M., Simeone, A., Gaggioli, V., Miyamoto, K., Allen, G.E., Erkek, S., Kwon, T., Marcotte, E.M., Zegerman, P

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PMID: 34023442 Ecotoxicol Environ SaflncRNA AABR07005593.1 potentiates PM2.5-induced interleukin-6 expression by targeting MCCC1

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Cell Ther

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