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Cellular Senescence in the Cardiovascular System: Molecular Mechanisms, Pathophysiology, and Senotherapeutic Interventions

Beata Franczyk1, Anna Bajer1,#, Anna Bulicz1,#, Mikołaj Grabarczyk1,#, Paulina Jakubowska1,#, Katarzyna Krawiranda1,#, Natalia Kustosik1,#, Przemysław Kuzar1,#, Klaudia Leszto1,#, Maja Mejza1,#, Weronika Mstowska1,#, Jacek Rysz2, Ewelina Młynarska1,*
1 Department of Nephrocardiology, Medical University of Lodz, Lodz, Poland
2 Department of Nephrology, Hypertension and Internal Medicine, Medical University of Lodz, Lodz, Poland
* Corresponding Author: Ewelina Młynarska. Email: email
# These authors contributed equally to this work
(This article belongs to the Special Issue: Cellular Senescence in Health and Disease)

BIOCELL https://doi.org/10.32604/biocell.2026.075767

Received 07 November 2025; Accepted 21 February 2026; Published online 09 March 2026

Abstract

Cellular senescence and the Senescence-Associated Secretory Phenotype (SASP) play both physiological and pathological roles in the cardiovascular system. While transient senescence aids regeneration, chronic accumulation of senescent cells promotes endothelial dysfunction, arterial stiffening, and maladaptive cardiac remodeling. This review elucidates the pivotal role of the immune system in senescent cell clearance and explores how immunosenescence drives systemic low-grade inflammation. Significant emphasis is placed on emerging pharmacological strategies, specifically senolytics and senomorphics, assessing their capacity to restore cardiac function and attenuate atherosclerosis. Additionally, the utility of molecular biomarkers and diverse in vitro and in vivo models is analyzed in the context of therapeutic efficacy. Ultimately, this article asserts that a comprehensive understanding of senescent-immune interactions is fundamental to the development of targeted, personalized interventions for age-related cardiovascular pathologies.

Keywords

Cellular senescence; cardiovascular aging; senolytics; senomorphics; cardiovascular system; heart failure; atherosclerosis; endothelial dysfunction
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