Ageing research reviewsMay 14, 2026

Cell Aging in Body Systems Linked to Heart and Blood Vessel Aging

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated May 15, 2026

Abstract

Cellular senescence may be a key driver of cardiovascular ageing influenced by complex interactions among various cell types.

Cardiovascular senescence is shaped by interactions among endothelial, vascular smooth muscle, immune, and stromal cells rather than being a uniform process.
Molecular hallmarks of cardiovascular senescence include DNA damage responses, telomere shortening, mitochondrial dysfunction, and changes in gene expression.
Key regulators integrate signals from oxidative stress, inflammation, and metabolic changes, potentially influencing senescence outcomes.
An inflammation-coagulation-senescence axis may help explain the relationship between chronic inflammation, arterial stiffening, and heart failure.
Emerging metabolic checkpoints in vascular smooth muscle cells may play a role in the initiation and progression of senescence.
Precision-guided interventions are needed to address the heterogeneity of senescence, considering factors like disease stage and cell type.

Simplified

Cellular senescence is increasingly recognized as a fundamental driver of cardiovascular ageing; however, its molecular heterogeneity, cell-type specificity, and translational relevance remain incompletely understood. Accumulating evidence indicates that cardiovascular senescence is not a uniform or cell-autonomous process, but rather an emergent property of interacting endothelial, vascular smooth muscle, immune, and stromal cell networks shaped by metabolic stress, immune dysregulation, and chromatin reorganization. In this review, we synthesize recent advances in the molecular hallmarks of cardiovascular senescence, including DNA damage responses, telomere attrition, mitochondrial dysfunction, SASP, and epigenetic remodeling, with an emphasis on how these features diverge across cardiovascular cell types. We highlight key transcriptional and post-transcriptional regulators as nodal integrators of oxidative stress, inflammation, and metabolic reprogramming. At the systems level, we propose an inflammation-coagulation-senescence axis to conceptualize how chronic inflammatory burden, immunothrombosis, arterial stiffening, and heart failure. We further discuss emerging metabolic checkpoints in vascular smooth muscle cell ageing, as modulators of senescence initiation and progression. Finally, we critically assess current senescence-targeted strategies emphasizing that their efficacy is constrained by senescence heterogeneity, disease stage, and context-dependent cellular interactions. Rather than supporting uniform anti-senescence approaches, accumulating evidence underscores the need for precision-guided interventions that account for temporal hierarchy, cell-type specificity, and metabolic state. We argue that integrating single-cell and spatial multi-omics with biological age metrics and machine-learning will be essential to define biologically vulnerable states, identify actionable therapeutic windows, and translate senescence biology into stage-specific and cell-targeted strategies for healthier cardiovascular ageing.

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Competing interests

Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

PubMed

Cell Aging in Body Systems Linked to Heart and Blood Vessel Aging

Abstract

Full Text

Funding

Competing interests

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