Endothelial cell senescence in aging-related vascular dysfunction
Open accessAbstract
Increased cardiovascular disease in aging is partly a consequence of the vascular endothelial cell (EC) senescence and associated vascular dysfunction. In this contest, EC senescence is a pathophysiological process of structural and functional changes including dysregulation of vascular tone, increased endothelium permeability, arterial stiffness, impairment of angiogenesis and vascular repair, and a reduction of EC mitochondrial biogenesis. Dysregulation of cell cycle, oxidative stress, altered calcium signaling, hyperuricemia, and vascular inflammation have been implicated in the development and progression of EC senescence and vascular disease in aging. A number of abnormal molecular pathways are associated with these underlying pathophysiological changes including Sirtuin 1, Klotho, fibroblast growth factor 21, and activation of the renin angiotensin-aldosterone system. However, the molecular mechanisms of EC senescence and associated vascular impairment in aging are not completely understood. This review provides a contemporary update on molecular mechanisms, pathophysiological events, as well functional changes in EC senescence and age-associated cardiovascular disease. This article is part of a Special Issue entitled: Genetic and epigenetic regulation of aging and longevity edited by Jun Ren & Megan Yingmei Zhang.
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This expression profile is indicative of an early cellular senescence phenotype.
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- Authors
- Jia, G., Aroor, A. R., Jia, C., & Sowers, J. R.
- Affiliations
- University of Missouri Health System (US)
- Corresponding author
- Jia, Guanghong
- Sowers, James R.
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
- Publisher
- Elsevier BV
- Published
- 2019-07
- Volume
- 1865
- Issue
- 7
- Pages
- 1802-1809
- ISSN
- 0925-4439 (ISSN-L)
- OpenAlex
- W2885972205
- Cited by
- 454
- References
- 96
- Citations by year
- 2026: 52 · 2025: 88 · 2024: 67 · 2023: 83 · 2022: 76 · 2021: 48 · 2020: 33 · 2019: 6
- FWCI
- 2.86
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Diabetes Association (1-17-IBS-201)
- NIH (R01 HL73101-01A, R01 HL107910-01)
- Veterans Affairs Merit System (0018)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
- Keywords
- endothelial cell senescence, vascular aging, vascular dysfunction, age-related cardiovascular disease, oxidative stress, calcium signaling, hyperuricemia, vascular inflammation, mitochondrial biogenesis, angiogenesis, arterial stiffness, endothelial permeability, SIRT1, Klotho, FGF21, renin-angiotensin-aldosterone system, cell cycle
- MeSH terms
- Aging, Animals, Cardiovascular Diseases, Endothelium, Vascular, Humans, Signal Transduction, Cellular Senescence, Oxidative Stress, Vascular Stiffness
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