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However, in COPD, these regulatory mechanisms may be compromised due to the persistent action of inflammatory mediators or exposure to environmental stressors, leading to a failure in the timely clearance of damaged mitochondria, which subsequently exacerbates the progression of COPD (Table 1)

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Although adult skeletal muscle is debatably post-mitotic [98], AR and androgenic regulation of cell cycle activity/exit in the prostate has opened discussions for comparing underlying mechanisms of AR-mediated determination and adaptation of AR-expressing SCs within the myofiber [86, 99, 100]

Cellular apoptosis and inflammatory markers were evaluated in NRK-52E cells and mouse primary tubular cells after hypoxia and reoxygenation using a hypoxia work station