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The theory is that cycling prevents receptor desensitization and reduces cumulative side effect burden

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It upregulates genes involved in collagen synthesis (COL1A1, COL3A1, COL5A1), extracellular matrix remodeling (decorin, fibromodulin), and antioxidant defense (superoxide dismutase, glutathione peroxidase) while simultaneously suppressing genes associated with inflammation (IL-6, TNF-alpha), fibrinogen production, and tissue destruction (several MMPs)

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Third, we did not investigate the cell cycle or apoptosis in the oxidative stress-induced senescence model

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