Journal of Volgograd State Medical University · Oct 15, 2026

Cellular senescence, early vascular aging syndrome and subclinical atherosclerosis in young adults: an umbrella review

By Lyamina S, Валерьевич КС, Павловна ЛН

In the last decade cell senescence is considered not only as a marker, but also as an active mechanism of early vascular aging (EVA) and atherogenesis. The aim of the research is to systemize and assess the prove of concept from systematic reviews, meta-analysis, prospective cohort and key primary studies concerning the role of cell senescence in the EVA and subclinical atherosclerosis pathogenesis in young adults, and about diagnostic value of instrumental and molecular methods in such patients. Research methodology: The umbrella review was carried out according the JBI guidelines and PRIOR recommendations7 The research was performed in PubMed/MEDLINE, Scopus, Web of Science, Cochrane CDSR and RSCI (eLIBRARY) for the period of 2008–2026 years. The methodology quality of the included reviews was assessed by AMSTAR-2, integrated proves – by GRADE system; the corrected covered area (CCA) was also assessed. The results of the research: Senescence in the vascular cells, realized by the pathways p53/p21, p16INK4a/Rb and cGAS-STING, generates proinflammatory secretory phenotype (SASP), which is connected with destabilization of the atherosclerotic plaque, increased arterial stiffness and accelerated atherogenesis. The most mature evidence supports instrumental EVA markers – carotid-femoral pulse wave velocity (cfPWV; EVA threshold ≥9.2 m/s in young adults) and the cardio-ankle vascular index (CAVI); carotid intima-media thickness (0.9 mm) serves as a surrogate of early atherosclerosis. Under standardised criteria EVA is detected in 10–27 % of individuals aged 18–30, and subclinical atherosclerosis in about 18.5 % of young adults. The most promising molecular markers are p16INK4a mRNA in T lymphocytes, leukocyte telomere length (LTL), GDF-15 and cystatin C. Conclusion: An integrative second-level review combining the molecular mechanisms of senescence, instrumental EVA diagnosis and data on young cohorts justifies priorities for prospective biomarker validation and the development of clinically applicable stratification models.

doi.org/10.19163/1994-9480-2026-23-3-38-48Open accessMechanisms