Single-cell transcriptomic studies reveal that arterial aging involves coordinated dysfunction across endothelial cells, smooth muscle cells, fibroblasts, and immune populations—characterized by senescence, matrix remodeling, and chronic inflammation. Understanding this cellular heterogeneity provides a foundation for identifying intervention points before structural arterial changes become irreversible.
Key Points
- Endothelial cells acquire pro-inflammatory phenotypes; smooth muscle transitions to synthetic states
- Fibroblasts increase matrix production and express antigen-presenting molecules during aging
- Persistent cellular stress from ROS and turnover drives premature senescence across cell types
Longevity Analysis
Arterial aging represents a cascade of cellular state changes rather than uniform decline—endothelial dysfunction precedes structural stiffening, smooth muscle phenotypic switching alters contractility, and fibroblast-driven matrix remodeling reduces arterial compliance. The emergence of senescent cells and chronic low-grade inflammation within the arterial wall directly undermines circulation and energy production efficiency. These findings suggest that intervention must address multiple cell populations simultaneously and that identifying senescence and inflammatory phenotypes before they accumulate offers a tractable target for slowing cardiovascular aging.
Original published by Wiley Aging Cell, by He Xu, Paul‐Lennard Mendez, Dimitri Kasakovski, Judith Sluimer .