<p>This narrative review synthesizes current evidence on the cellular stress mechanisms that drive apoptosis in cochlear hair cells during age-related hearing loss (ARHL). A total of 49 studies were screened, of which 32 met eligibility criteria and were included. Most studies employed mouse, rat, guinea pig, or chinchilla models, in combination with in vitro cell lines and explant cultures. Oxidative stress emerged as the most consistently reported mechanism, described in 21 studies, with reactive oxygen species, SIRT1/3 signaling, Nrf2, and microRNAs mediating mitochondrial dysfunction and DNA damage that initiate both intrinsic and extrinsic apoptotic pathways. Endoplasmic reticulum stress, reported in five studies, contributed to unfolded protein response activation, calcium dysregulation, and pro-apoptotic signaling through CHOP and GRP78. Four studies identified mitochondrial dysfunction, with loss of membrane potential, ATP depletion, and cytochrome c release as hallmarks leading to intrinsic apoptosis. Additional processes, including autophagy, ferroptosis, and necroptosis, were reported in select models, indicating a broader spectrum of regulated cell death mechanisms. Interventions such as antioxidants, SIRT activators, and autophagy modulators were shown to attenuate hair cell death in preclinical models. Collectively, the findings indicate that oxidative stress and mitochondrial dysfunction are central drivers of hair cell apoptosis, while ER stress and emerging mechanisms like ferroptosis provide further mechanistic insight. These stress pathways converge to promote apoptosis, underscoring potential therapeutic targets for ARHL.</p>