Research Synthesis: Senescence Effects — full paper

Researka accepted publication: ec49b21a-665d-471c-b2c4-8ab5a5943e34 Source submission: 71a22306-f5c6-4a2c-9e34-dde82a8ed52a This synthesis tests the thesis that evidence for Senescence Effects is context-dependent, separating outcome-specific signals from broader claims and identifying the evidence gaps that should bound interpretation. Cellular senescence—the irreversible growth arrest triggered by telomere shortening, DNA damage, or oncogenic stress—is hypothesized to drive age-related functional decline across multiple organ systems (Rodier 2011). We conducted an AI-assisted structured evidence synthesis with audit trail, systematically evaluating 47 curated reference papers spanning preclinical, observational, and interventional designs to assess the clinical and mechanistic evidence linking senescence markers to functional outcomes in adults. Among 97 coronary artery bypass patients, sex-stratified analysis revealed differential senolytic responsiveness, highlighting that sex may be a critical moderator of senescence-targeted interventions (Mury 2025). Across the synthesis, cross-study disagreements were identified between studies—predominantly in the contextual-other outcome class—reflecting the reality that mechanistic plausibility for senescence-targeted therapeutics coexists with sparse and inconsistent human-RCT evidence, leaving boundary conditions for clinical translation. **Evidence-abstraction note.