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10.4081/ejtm.2022.10416 13 FalckenhaynC.BienkowskaA.ShleJ.WegnerK.RaddatzG.KristofB.et al (2024)

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[69] showed that the activation of AMPK can inhibit the mammalian target of rapamycin (mTOR), resulting in the blockade of the synthesis of downstream proteins

Experimental studies have demonstrated that aerobic exercise can preserve mitochondrial metabolism by preventing age-related mitochondrial damage in skeletal muscle, achieved through inhibiting mitochondrial schizopyranin expression in a PGC-1-dependent manner (146)

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These molecules activate and recruit immune cells (M1 macrophages, neutrophils, Th17 cells), which in turn exacerbate oxidative stress and iron dysregulation, creating a self-amplifying cycle