# The Role of Cellular Senescence and SASP in the Pathogenesis of Atherosclerosis and the Therapeutic Potential of Senolytic Strategies in Cardiovascular Diseases

## TL;DR

This paper explores how cellular aging contributes to heart disease and how targeting aged cells might help treat it.

## Contribution

The paper provides a comprehensive overview of how cellular senescence and SASP contribute to atherosclerosis and evaluates emerging senolytic therapies.

## Key findings

- Cellular senescence and SASP contribute to chronic inflammation and plaque instability in atherosclerosis.
- Senolytic therapies show potential in reducing vascular inflammation and stabilizing plaques.
- Immunosenolytic and epigenetic approaches are emerging as promising therapeutic strategies.

## Abstract

Cellular senescence is a permanent cell cycle arrest that plays a critical role in the development and pathogenesis of age-related diseases. This paper aims to present the biological mechanisms of cellular senescence and the role of the senescence-associated secretory phenotype (SASP) in the pathogenesis of atherosclerosis, as well as to discuss therapeutic strategies targeting senescent cells in cardiovascular diseases. Different types of cellular senescence are described, including replicative, stress-induced, and oncogene-induced senescence, along with the composition and regulation of SASP and its impact on chronic inflammation, endothelial dysfunction, vascular remodeling, and plaque destabilization. The involvement of senescent endothelial cells, vascular smooth muscle cells, and macrophages in the initiation and progression of atherosclerosis is also discussed. The paper reviews current research on senolytic and senomorphic therapies and highlights emerging approaches such as immunosenolytic and epigenetic interventions. The therapeutic potential of these strategies in reducing chronic vascular inflammation and improving plaque stability, as well as their limitations and challenges in clinical application, is emphasized.