Abel Martin Garrido1, Martin Bennett. 1. Division of Cardiovascular Medicine, University of Cambridge, Box 110, Addenbrooke's Centre for Clinical Investigation, Addenbrooke's Hospital, Cambridge, UK.
Abstract
PURPOSE OF REVIEW: Cell senescence is a major process regulating tissue mass, architecture and function, and underlies many diseases of ageing. Recent studies have elucidated some of the regulatory pathways leading to cell senescence, and senescence has also been found in the vasculature. However, assessment of cell senescence is problematic, and the effects of vascular cell senescence are in most cases unproven. The present article will review how senescence is assessed, how it is regulated, where senescence has been described, and the role of cell senescence in atherosclerosis. RECENT FINDINGS: Senescence results in expression of multiple proteins, both intracellular and secreted. However, to date, none of these are specific for senescence, and multiple markers must be used together for positive identification. Despite these shortfalls, cell senescence is detectable in the vasculature in ageing and in human atherosclerosis, and recent studies in mice have indicated that cell senescence promotes both atherogenesis and multiple features of 'vulnerable' lesions in advanced atherosclerotic plaques. SUMMARY: The almost ubiquitous presence of cell senescence in atherosclerosis and the fundamental role of senescence in regulating plaque development and stability suggest that prevention or amelioration of senescence in atherosclerosis is a viable therapeutic target.
PURPOSE OF REVIEW: Cell senescence is a major process regulating tissue mass, architecture and function, and underlies many diseases of ageing. Recent studies have elucidated some of the regulatory pathways leading to cell senescence, and senescence has also been found in the vasculature. However, assessment of cell senescence is problematic, and the effects of vascular cell senescence are in most cases unproven. The present article will review how senescence is assessed, how it is regulated, where senescence has been described, and the role of cell senescence in atherosclerosis. RECENT FINDINGS: Senescence results in expression of multiple proteins, both intracellular and secreted. However, to date, none of these are specific for senescence, and multiple markers must be used together for positive identification. Despite these shortfalls, cell senescence is detectable in the vasculature in ageing and in humanatherosclerosis, and recent studies in mice have indicated that cell senescence promotes both atherogenesis and multiple features of 'vulnerable' lesions in advanced atherosclerotic plaques. SUMMARY: The almost ubiquitous presence of cell senescence in atherosclerosis and the fundamental role of senescence in regulating plaque development and stability suggest that prevention or amelioration of senescence in atherosclerosis is a viable therapeutic target.