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

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

Sezin T, Krajewski M, Wutkowski A, Mousavi S, Chakievska L, Bieber K, et al

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

Anti-inflammatory functions of trimetazidine Preclinical studies Neutrophils are a key part of the immune system as the major type of white blood cells [147]