Literature DB >> 25171100

Proinflammation of aging central arteries: a mini-review.

Mingyi Wang1, Robert E Monticone, Edward G Lakatta.   

Abstract

Arterial aging is a cornerstone of organismal aging. The central arterial wall structurally and functionally remodels under chronic proinflammatory stress over a lifetime. The low-grade proinflammation that accompanies advancing age causes arterial wall thickening and stiffening. These structural and functional alterations are consequences of adverse molecular and cellular events, e.g. an increase in local angiotensin II signaling that induces an inflammatory phenotypic shift of endothelial and smooth muscle cells. Thus, interventions to restrict proinflammatory signaling are a rational approach to delay or prevent age-associated adverse arterial remodeling.
© 2014 S. Karger AG, Basel.

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Year:  2014        PMID: 25171100      PMCID: PMC4209183          DOI: 10.1159/000362548

Source DB:  PubMed          Journal:  Gerontology        ISSN: 0304-324X            Impact factor:   5.140


  81 in total

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4.  Angiotensin II activates matrix metalloproteinase type II and mimics age-associated carotid arterial remodeling in young rats.

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5.  Short communication: vascular smooth muscle cell stiffness as a mechanism for increased aortic stiffness with aging.

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10.  Involvement of NADPH oxidase in age-associated cardiac remodeling.

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Review 8.  Aging: Molecular Pathways and Implications on the Cardiovascular System.

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Review 10.  "Inflammaging" as a Druggable Target: A Senescence-Associated Secretory Phenotype-Centered View of Type 2 Diabetes.

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