Key result
Vascular stiffness markers detect early vascular aging in up to ~27% of young adults.
Why the study?
Cell senescence is increasingly considered an active mechanism of early vascular aging and atherogenesis, requiring systematic assessment of its pathogenic role and the diagnostic value of instrumental and molecular methods in young adults.
Systematic Review
This umbrella review synthesizes molecular and instrumental evidence linking cellular senescence to early vascular aging and subclinical atherosclerosis in young adults, identifying key biomarkers (such as cfPWV, CAVI, p16INK4a, LTL, GDF-15, and cystatin C) for future risk stratification models.
Supports awareness of early vascular aging in young adults; leaves open prospective validation of senescence biomarkers for risk models.
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.
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Lyamina et al. (2026) conducted a systematic review in Early vascular aging (EVA) and subclinical atherosclerosis. Cellular senescence and diagnostic markers (cfPWV, CAVI, cIMT, p16INK4a, LTL, GDF-15, cystatin C) was evaluated on Prevalence and pathogenesis of early vascular aging (EVA) and subclinical atherosclerosis. Standardized vascular senescence and stiffness markers (e.g., cfPWV ≥9.2 m/s) detect early vascular aging in 10–27% of adults aged 18–30 and subclinical atherosclerosis in ~18.5%.
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