TY - JOUR
T1 - Proinflammation
T2 - The key to arterial aging
AU - Wang, Mingyi
AU - Jiang, Liqun
AU - Monticone, Robert E.
AU - Lakatta, Edward G.
N1 - Funding Information:
This research was supported by the Intramural Research Program of the National Institute on Aging, National Institutes of Health.
PY - 2014/2
Y1 - 2014/2
N2 - 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.
AB - 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.
KW - Angiotensin II
KW - Atherosclerosis
KW - Central arterial aging
KW - Hypertension
KW - Proinflammation
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U2 - 10.1016/j.tem.2013.10.002
DO - 10.1016/j.tem.2013.10.002
M3 - Review article
C2 - 24365513
AN - SCOPUS:84892967417
SN - 1043-2760
VL - 25
SP - 72
EP - 79
JO - Trends in Endocrinology and Metabolism
JF - Trends in Endocrinology and Metabolism
IS - 2
ER -