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These synergistic mechanisms collectively highlight exercise as a potent intervention against ferroptosis-induced cellular damage, thereby providing therapeutic potential for a range of ferroptosis-associated diseases

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Several mechanisms have been proposed to explain this: (i) bystander apoptosis occurs due to viral proteins promoting the apoptosis of nearby cells (notably HIV-1 gp120 after its interactions with CD4+ and CCR5 or CXCR4 coreceptors), (ii) immune activation induces FasL production and Fas (CD95) expression in nearby, uninfected CD4+ T cells, resulting in shortened lifespans and an increased sensibility to activation-induced cell death (AICD), and (iii) abortive infection leading to pyroptosis through the caspase-1 pathway, due to an accumulation of incomplete reverse transcripts and the induction of antiviral and inflammatory responses [11]