Abstract

Atherosclerosis is probably one of the paradigms of disease linked to aging. Underlying the physiopathology of atherosclerosis are cellular senescence, oxidative stress, and inflammation. These factors are increased in the elderly and from chronic disease patients. Elevated levels of oxidative stress affect cellular function and metabolism, inducing senescence. This senescence modifies the cell phenotype into a senescent secretory phenotype. This phenotype activates immune cells, leading to chronic systemic inflammation. Moreover, due to their secretory phenotype, senescence cells present an increased release of highlighted extracellular vesicles that will change nearby/neighborhood cells and paracrine signaling. For this reason, searching for specific senescent cell biomarkers and therapies against the development/killing of senescent cells has become relevant. Recently, senomorphic and senolityc drugs have become relevant in slowing down or eliminating senescence cells. However, even though they have shown promising results in experimental studies, their clinical use is still yet to be determined.

Highlights

  • Atherosclerosis is the most common cardiovascular system disorder characterized by atheroma’s plaque formation on arterial walls [1]

  • Artery plaque formation is a progressive disorder initiated by damage accumulation in the artery and influenced by cardiovascular risk factors [1], including age, which is a universal factor for arteriosclerosis development [3]

  • Several clinical and experimental studies have suggested that the physiopathology of this age-related disease is associated with the physiological process of cellular senescence, which is activated in damage associated with stressful situations in all types of cells, as shown in tumor formation [9]

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Summary

Introduction

Atherosclerosis is the most common cardiovascular system disorder characterized by atheroma’s plaque formation on arterial walls [1]. One common hallmark of these age-related diseases is cellular senescence [8] In this regard, several clinical and experimental studies have suggested that the physiopathology of this age-related disease is associated with the physiological process of cellular senescence, which is activated in damage associated with stressful situations in all types of cells, as shown in tumor formation [9]. The aging process is associated with a frailty situation in which old adults impair the physiological homeostatic system, which cannot respond successfully to stressful situations. This frailty state is reached when tissues and systems fail because their cells have become senescent due to damage accumulation over the years or by damaging agents in chronic pathologies [3]. Likewise, knowing how and why the senescent cell acts as a pathophysiological mechanism in developing age-specific diseases offers new approaches to early diagnosis and the possibility of new therapeutic strategies based on the control of cellular senescence

Cellular Senescence
Factors That Induce Endothelial Senescence
Low Degree Chronic Systemic Inflammation as a Key Risk Factor of Endothelial Senescence
Extracellular Vesicles and Endothelial Senescence

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