The 2026 Aging-US review by Deng and Yang reframes cellular senescence not as uniform pathology but as a context-dependent process, synthesizing mechanisms across organs like liver, brain, and skin where stressors such as telomere attrition and oxidative damage trigger arrest. Unlike blanket 'zombie cell' eradication narratives in popular coverage, this peer-reviewed literature review (not a primary study with patient cohorts) highlights functional heterogeneity: some senescent populations secrete SASP factors that promote wound closure and limit fibrosis, while others drive chronic inflammation. A critical gap in the source is its limited engagement with longitudinal human data; most cited evidence derives from rodent models and in vitro work, which often overstate clearance benefits due to species-specific immune responses. Synthesizing with Demaria et al. (Dev Cell, 2014; mouse wound-healing assays, n=small cohorts) reveals senescence-derived PDGF-AA as essential for optimal repair—ablating these cells impaired healing, a finding echoed in Baker et al. (Nature, 2016; genetic clearance models showing mixed outcomes on tissue regeneration). This opens precision pathways like marker-specific CAR-T or senomorphics that spare beneficial subsets, challenging early dasatinib-quercetin trials that ignored regenerative trade-offs. Limitations include publication bias toward harmful phenotypes in pre-2020 literature and absence of large-scale human senolytic RCTs, urging caution in translating to clinical anti-aging protocols.