A Primate‐Specific <scp> lncRNA <i>LINC01021</i> </scp> Contributes to Cellular and Organismal Aging via <scp>DAZAP1</scp> ‐Dependent Destabilization of <scp>RBMX</scp>

Aging is characterized by progressive physiological decline and age-related pathologies, yet the molecular determinants underlying lineage- and species-specific aging traits remain poorly understood. Although protein-coding regulators have dominated aging research, the contribution of long non-coding RNAs (lncRNAs), particularly primate-specific lncRNAs, has not been systematically explored. Here, through evolutionary screening and cross-species aging-associated analyses, we identified a set of primate-specific lncRNAs (including LINC01021, CTC-575 l10.1, CTA-150C2.13, and RP11-305F18.1, etc.) associated with human aging, and we functionally characterized LINC01021 as a representative candidate to assess their causal involvement. In human cells, LINC01021 promotes cellular senescence, whereas its silencing attenuates senescence-associated phenotypes. Mechanistically, LINC01021 is predominantly located in the nucleus, where it facilitates DAZAP1-dependent destabilization of RBMX mRNA, leading to activation of the P53 pathway and induction of canonical senescence features. At the organismal level, ectopic expression of human LINC01021 in mice contributes to aging-like phenotypes, including increased frailty and impaired motor coordination. Together, these findings implicate primate-specific lncRNAs in lineage-restricted aging and highlight an evolutionarily recent regulatory layer that may modulate aging trajectories.