Factors and Pathways Modulating Endothelial Cell Senescence in Vascular Aging

Aging causes a progressive decline in the structure and function of organs. With advancing age, an accumulation of senescent endothelial cells (ECs) contributes to the risk of developing vascular dysfunction and cardiovascular diseases, including hypertension, diabetes, atherosclerosis, and neurodeg...

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Veröffentlicht in:International journal of molecular sciences Jg. 23; H. 17; S. 10135
Hauptverfasser: Hwang, Hyun Jung, Kim, Nayeon, Herman, Allison B., Gorospe, Myriam, Lee, Jae-Seon
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Basel MDPI AG 04.09.2022
MDPI
Schlagworte:
Age
Aging
Apoptosis
Atherosclerosis
Autophagy
Cardiovascular disease
Cell cycle
Chemokines
Coronary vessels
Cyclin-dependent kinases
Cytokines
DNA damage
Endothelium
Enzymes
Hypertension
Kinases
Metabolism
Mitochondria
Nitric oxide
Oxidative stress
Phosphorylation
Physiology
Polyploidy
Proteins
Review
Veins & arteries
ISSN:1422-0067, 1661-6596, 1422-0067
Online-Zugang:Volltext
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Zusammenfassung:Aging causes a progressive decline in the structure and function of organs. With advancing age, an accumulation of senescent endothelial cells (ECs) contributes to the risk of developing vascular dysfunction and cardiovascular diseases, including hypertension, diabetes, atherosclerosis, and neurodegeneration. Senescent ECs undergo phenotypic changes that alter the pattern of expressed proteins, as well as their morphologies and functions, and have been linked to vascular impairments, such as aortic stiffness, enhanced inflammation, and dysregulated vascular tone. Numerous molecules and pathways, including sirtuins, Klotho, RAAS, IGFBP, NRF2, and mTOR, have been implicated in promoting EC senescence. This review summarizes the molecular players and signaling pathways driving EC senescence and identifies targets with possible therapeutic value in age-related vascular diseases.
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ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms231710135