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Endothelial aging
Abstract
Aging is considered to be the major risk factor for the development of atherosclerosis and, therefore, for coronary artery disease. Apart from age-associated remodeling of the vascular wall, which includes luminal enlargement, intimal and medial thickening, and increased vascular stiffness, endothelial function declines with age. This is most obvious from the attenuation of endothelium-dependent dilator responses, which is a consequence of the alteration in the expression and/or activity of the endothelial NO synthase, upregulation of the inducible NO synthase, and increased formation of reactive oxygen species. Aging is also associated with a reduction in the regenerative capacity of the endothelium and endothelial senescence, which is characterized by an increased rate of endothelial cell apoptosis.
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“we used a well-established model for endothelial aging57,58 by generating human induced pluripotent stem cells (hiPSCs) from fibroblasts obtained from five independent human donors59 and subsequently differentiated them into endothelial cells (hiPSC-ECs)60.”
From An inflammatory aging clock (iAge) based on deep learning tracks multimorbidity, immunosenescence, frailty and cardiovascular aging (2021) · cites this paper as [58]
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Items 101–107 of 107
Vascular aging: implications for cardiovascular disease and therapy
Ghebre, Y. T., Yakubov, E., Wong, W. T., & Krishnamurthy, P. (2016) · Translational Medicine · doi:10.4172/2161-1025.1000183 · Cited by 87
“With advancing age, ECs have depleted anti-inflammatory and antioxidant defense mechanisms and are subjected to augmented inflammatory and oxidative stress that impairs their number, morphology and function [11].”
BackgroundInorganic nitrite supplementation for healthy arterial aging
Sindler, A. L., DeVan, A. E., Fleenor, B. S., & Seals, D. R. (2014) · Journal of Applied Physiology · doi:10.1152/japplphysiol.01100.2013 · Cited by 68
“, superoxide dismutases; SOD) are among the key players contributing to oxidative stress, reduced NO, and vascular dysfunction with aging (15, 64, 130).”
BackgroundKim, I.-Y., Schutzler, S. E., Schrader, A., Spencer, H. J., Azhar, G., Deutz, N. E. P., & Wolfe, R. R. (2015) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00339.2015 · Cited by 67
“This condition is commonly referred to as endothelial dysfunction (12).”
BackgroundInfluentialRedox Characterization of Functioning Skeletal Muscle
Zuo, L., & Pannell, B. K. (2015) · Frontiers in Physiology · doi:10.3389/fphys.2015.00338 · Cited by 60
“Other potential effects exerted by ROS may include DNA damage, decreased mitochondria function, dysfunctional polypeptides, reduced muscle contractile force, and loss of muscle mass (Brandes et al., 2005; Shi et al., 2013).”
BackgroundProtective effect of extracellular superoxide dismutase on endothelial function during aging
Lund, D. D., Chu, Y., Miller, J. D., & Heistad, D. D. (2009) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.01342.2008 · Cited by 56
Endothelial function and the regulation of muscle protein anabolism in older adults
Timmerman, K. L., & Volpi, E. (2013) · Nutrition, Metabolism and Cardiovascular Diseases · doi:10.1016/j.numecd.2012.03.013 · Cited by 53
Why the endothelium? The endothelium as a target to reduce diabetes-associated vascular disease
Triggle, C. R., Ding, H., Marei, I., Anderson, T. J., & Hollenberg, M. D. (2020) · Canadian Journal of Physiology and Pharmacology · doi:10.1139/cjpp-2019-0677 · Cited by 49
Metadata
- Authors
- BRANDES, R., FLEMING, I., & BUSSE, R.
- Affiliations
- Goethe University Frankfurt (DE)
- Corresponding author
- BRANDES, R
- ORCID
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2005-05-01
- Volume
- 66
- Issue
- 2
- Pages
- 286-294
- ISSN
- 0008-6363 (ISSN-L)
- OpenAlex
- W4256530495
- Cited by
- 563
- References
- 0
- Citations by year
- 2026: 13 · 2025: 19 · 2024: 23 · 2023: 23 · 2022: 38 · 2021: 31 · 2020: 27 · 2019: 26 · 2018: 20 · 2017: 26 · 2016: 32 · 2015: 33 · 2014: 35 · 2013: 25 · 2012: 41
- FWCI
- 12.98
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cardiovascular Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Keywords
- endothelial aging, endothelial function, atherosclerosis, coronary artery disease, nitric oxide synthase, inducible nitric oxide synthase, reactive oxygen species, endothelial cell senescence, endothelial cell apoptosis, vascular remodeling, vascular stiffness
- MeSH terms
- Aged, Aging, Coronary Disease, Endothelium, Vascular, Humans, Vasodilation, Cellular Senescence, Apoptosis, Reactive Oxygen Species, Oxidative Stress, Nitric Oxide Synthase, Nitric Oxide Synthase Type II, Nitric Oxide Synthase Type III
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