Cellular Senescence, Inflammaging and Cardiovascular Disease

TL;DR

This paper reviews how aging-related processes like cellular senescence and chronic inflammation contribute to cardiovascular disease and explores potential therapies.

Contribution

The paper provides a comprehensive review of how inflammaging and cellular senescence drive cardiovascular aging and highlights emerging therapeutic strategies.

Findings

Cellular senescence and SASP contribute to chronic inflammation and tissue remodeling in aging.

Macrophages play a key role in clearing senescent cells, impacting cardiovascular health.

Drugs like metformin may offer cardiovascular benefits through anti-aging mechanisms.

Abstract

Aging is the most important yet unmodifiable risk factor for cardiovascular disease (CVD). As a result, targeting cardiovascular aging has emerged as a promising strategy to promote long‐term cardiovascular health. This review summarizes current knowledge on the effects of aging within the cardiovascular system as well as systemic processes that modulate them. We highlight the roles of cellular senescence and the senescence‐associated secretory phenotype (SASP), emphasizing their heterogeneous contributions to chronic low‐grade inflammation and tissue remodeling—collectively termed inflammaging. Advances in biomarkers, animal models, and systems biology approaches have deepened our understanding of the interplay between senescence, inflammaging, and cardiovascular dysfunction, including the pivotal role of macrophages in senescent cell clearance. Therapeutic strategies are diverse, ranging from senolytic approaches designed to selectively eliminate senescent cells, to SASP modulation, and interventions targeting chronic inflammation and metabolic dysregulation. Of particular interest, drugs already in clinical use—such as metformin and other anti‐diabetic agents—show beneficial effects on aging‐related pathways, suggesting that their cardiovascular protection may in part reflect anti‐aging properties. Despite these advances, therapies directly targeting senescence and inflammaging to reduce the global burden of CVD remain an urgent unmet need.

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