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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Bibliographic Details
Published in:International journal of molecular sciences 2022-09, Vol.23 (17), p.10135
Main Authors: Hwang, Hyun Jung, Kim, Nayeon, Herman, Allison B., Gorospe, Myriam, Lee, Jae-Seon
Format: Article
Language:English
Subjects:
Age
age-related vascular disease
Aging
Aorta
Apoptosis
Arteriosclerosis
Atherosclerosis
Autophagy
Cardiovascular disease
Cardiovascular diseases
Cell cycle
cellular senescence
Chemokines
Coronary vessels
Cyclin-dependent kinases
Cytokines
Diabetes mellitus
DNA damage
endothelial cell
Endothelial cells
Endothelium
Enzymes
Hypertension
Kinases
Klotho protein
Metabolism
Mitochondria
molecular player
Neurodegeneration
Nitric oxide
Oxidative stress
Phosphorylation
Physiology
Polyploidy
Proteins
putative target
Review
Senescence
signaling pathway
Sirtuins
Stiffness
Structure-function relationships
TOR protein
Vascular diseases
Veins & arteries
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Summary: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.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms231710135