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- W2885454748 endingPage "223" @default.
- W2885454748 startingPage "210" @default.
- W2885454748 abstract "Age-associated structural and functional remodeling of the arterial wall produces a productive environment for the initiation and progression of hypertension and atherosclerosis. Chronic aging stress induces low-grade proinflammatory signaling and causes cellular proinflammation in arterial walls, which triggers the structural phenotypic shifts characterized by endothelial dysfunction, diffuse intimal-medial thickening, and arterial stiffening. Microscopically, aged arteries exhibit an increase in arterial cell senescence, proliferation, invasion, matrix deposition, elastin fragmentation, calcification, and amyloidosis. These characteristic cellular and matrix alterations not only develop with aging but can also be induced in young animals under experimental proinflammatory stimulation. Interestingly, these changes can also be attenuated in old animals by reducing low-grade inflammatory signaling. Thus, mitigating age-associated proinflammation and arterial phenotype shifts is a potential approach to retard arterial aging and prevent the epidemic of hypertension and atherosclerosis in the elderly." @default.
- W2885454748 created "2018-08-22" @default.
- W2885454748 creator A5020415713 @default.
- W2885454748 creator A5026735382 @default.
- W2885454748 creator A5077932215 @default.
- W2885454748 date "2018-01-01" @default.
- W2885454748 modified "2023-10-13" @default.
- W2885454748 title "Proinflammatory Arterial Stiffness Syndrome: A Signature of Large Arterial Aging" @default.
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