Journal
NATURE REVIEWS CARDIOLOGY
Volume 15, Issue 9, Pages 555-565Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41569-018-0030-z
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Funding
- AHA
- US National Institute on Aging [R01-AG055395, R01-AG047879, R01-AG038747, P30-AG050911, R01AG049821]
- US National Institute of Neurological Disorders and Stroke [R01-NS056218, R01-NS100782]
- US National Heart, Lung, and Blood Institute [R01-HL111178, R01-HL134778]
- Oklahoma Center for the Advancement of Science and Technology
- Presbyterian Health Foundation
- National Institute on Aging [T32AG052363]
- EU [EFOP-3.6.1-16-2016-0008]
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Ageing is the main risk factor for the development of cardiovascular diseases. A central mechanism by which ageing promotes vascular pathologies is compromising endothelial health. The age-related attenuation of endothelium-dependent dilator responses (endothelial dysfunction) associated with impairment of angiogenic processes and the subsequent pathological remodelling of the microcirculation contribute to compromised tissue perfusion and exacerbate functional decline in older individuals. This Review focuses on cellular, molecular, and functional changes that occur in the endothelium during ageing. We explore the links between oxidative and nitrative stress and the conserved molecular pathways affecting endothelial dysfunction and impaired angiogenesis during ageing. We also speculate on how these pathological processes could be therapeutically targeted. An improved understanding of endothelial biology in older patients is crucial for all cardiologists because maintenance of a competently functioning endothelium is critical for adequate tissue perfusion and long-term cardiac health.
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