title: Proinflammation: the key to arterial aging.
abstract: Arterial aging is the major contributing factor to increases in the incidence and prevalence of cardiovascular disease, due mainly to the presence of chronic, low-grade, 'sterile' arterial inflammation. Inflammatory signaling driven by the angiotensin II cascade perpetrates adverse age-associated arterial structural and functional remodeling. The aged artery is characterized by endothelial disruption, enhanced vascular smooth muscle cell (VMSC) migration and proliferation, extracellular matrix (ECM) deposition, elastin fracture, and matrix calcification/amyloidosis/glycation. Importantly, the molecular mechanisms of arterial aging are also relevant to the pathogenesis of hypertension and atherosclerosis. Age-associated arterial proinflammation is to some extent mutable, and interventions to suppress or delay it may have the potential to ameliorate or retard age-associated arterial diseases.
authors.affiliation: Laboratory of Cardiovascular Science, National Institution on Aging, National Institutes of Health, Biomedical Research Center (BRC), 251 Bayview Boulevard, Baltimore, MD 21224, USA. Electronic address: mingyiw@grc.nia.nih.gov.
authors.forename: Mingyi
authors.initials: M
authors.lastname: Wang
authors.affiliation: Laboratory of Cardiovascular Science, National Institution on Aging, National Institutes of Health, Biomedical Research Center (BRC), 251 Bayview Boulevard, Baltimore, MD 21224, USA.
authors.forename: Liqun
authors.initials: L
authors.lastname: Jiang
authors.affiliation: Laboratory of Cardiovascular Science, National Institution on Aging, National Institutes of Health, Biomedical Research Center (BRC), 251 Bayview Boulevard, Baltimore, MD 21224, USA.
authors.forename: Robert E
authors.initials: RE
authors.lastname: Monticone
authors.affiliation: Laboratory of Cardiovascular Science, National Institution on Aging, National Institutes of Health, Biomedical Research Center (BRC), 251 Bayview Boulevard, Baltimore, MD 21224, USA. Electronic address: lakattae@grc.nia.nih.gov.
authors.forename: Edward G
authors.initials: EG
authors.lastname: Lakatta
mesh_terms: D000368:Aged; D000375:Aging / Q000502:physiology*; D000804:Angiotensin II / Q000502:physiology; D000818:Animals; D000954:Antigens, Surface / Q000502:physiology; D001158:Arteries; D001167:Arteritis / Q000503:physiopathology; D050197:Atherosclerosis / Q000209:etiology*; D002154:Calpain / Q000502:physiology; D018932:Chemokine CCL2 / Q000502:physiology; D019332:Endothelin-1 / Q000502:physiology; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D007249:Inflammation / Q000503:physiopathology*; D018836:Inflammation Mediators / Q000502:physiology; D020778:Matrix Metalloproteinase 2 / Q000502:physiology; D008875:Middle Aged; D008894:Milk Proteins; D009131:Muscle, Smooth, Vascular / Q000473:pathology; D009569:Nitric Oxide / Q000502:physiology; D017382:Reactive Oxygen Species / Q000378:metabolism; D054390:Receptors, CCR2 / Q000502:physiology; D053773:Transforming Growth Factor beta1 / Q000502:physiology
chemical_list: D000954:Antigens, Surface; C111835:CCL2 protein, human; C515334:CCR2 protein, human; D018932:Chemokine CCL2; D019332:Endothelin-1; D018836:Inflammation Mediators; C098942:MFGE8 protein, human; D008894:Milk Proteins; D017382:Reactive Oxygen Species; D054390:Receptors, CCR2; D053773:Transforming Growth Factor beta1; D000804:Angiotensin II; D009569:Nitric Oxide; D002154:Calpain; C527669:CAPNS1 protein, human; D020778:Matrix Metalloproteinase 2
keywords: angiotensin II; atherosclerosis; central arterial aging; hypertension; proinflammation