ArticleClinical and translational medicine2026
NAT10-mediated N4-acetylcytidine modification drives RNA splicing of PML to alleviate adipose-derived stem cell senescence and promote diabetic wound healing.
Article in Clinical and translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundCellular senescence of adipose-derived stem cells (ADSCs) compromises their therapeutic potential in diabetic wound healing. Alternative splicing produces functionally different variants and serves as a critical regulator of senescence. N-acetyltransferase 10 (NAT10) is known to catalyse N4-acetylcytidine (ac4C) RNA modification, and ac4C modification has been involved in RNA splicing. Nevertheless, how NAT10 functions in ADSCs remain unexplored. The aim of this study was to investigate the involvement of NAT10 in ADSC senescence and its impact on RNA splicing.
methodsSenescence was assessed by β-galactosidase staining, western blot analysis of p21 and p16 and qRT-PCR detection of senescence-associated secretory phenotype (SASP) genes. The role of NAT10 in splicing regulation was examined by RT‑PCR.
resultsNAT10 overexpression mitigated ADSC senescence under high-glucose conditions and augmented the wound repair capability of ADSCs. Mechanistically, NAT10 facilitated ac4C-dependent AS of the PML transcript, driving a switch from the long isoform (PML-FL) to the short isoform (PML-S). PML-FL accelerated cellular senescence, whereas PML-S suppressed it. NAT10 recruited SRSF1 to PML pre-mRNA, leading to ac4C-SRSF1-mediated exon skipping and increased PML-S production. Concurrently, NAT10 reduced the binding of PCBP1 to PML, thereby inhibiting PML-FL generation.
conclusionsOur findings uncover a previously unrecognised mechanism by which NAT10 regulates ADSC senescence through ac4C-dependent alternative splicing and suggest a potential strategy to improve ADSC-based therapies for diabetic wounds. KEY POINTS: NAT10 catalyzes ac4C-dependent alternative splicing of PML pre-mRNA, shifting the balance from the pro-senescence PML-FL isoform to the protective PML-S isoform.
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