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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)

[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

Healthcare (Basel) 9

The range of these signaling pathways is constantly updated and expanded upon, and they may have complex intersections and interactions

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