Role of NFκB in age-related vascular endothelial dysfunction in humans
Year: 2009
Type: article
Abstract: Cardiovascular diseases (CVD) are the leading cause of morbidity and mortality in the United States and other industrialized societies.Older age is the major risk factor for development of CVD [1].Emerging evidence over the past 20 years suggests that the arterial vascular endothelium plays a critical role in the development of CVD, most notably, atherosclerosis.A healthy vascular endothelium is characterized by a tightly regulated balance of pro-and anti-oxidants, vasodilators and vasoconstrictors, and pro-and anti-inflammatory molecules.A diseased or dysfunctional endothelium displays a "pro-atherogenic" phenotype, losing its tightly regulated balance and adopting a prooxidant/vasoconstrictor/pro-inflammatory phenotype.A hallmark of arterial endothelial dysfunction is impaired endothelial dependent dilation, which is predictive of future CVD events [1,2].Aging leads to impaired endothelial dependent dilation associated elevated oxidative stress and a proinflammatory endothelial cell phenotype.Recent studies in humans by our group and by others in rodents suggest a critical role of nuclear factor κB (NFκB) in the pro-inflammatory / pro-oxidant linked suppression of endothelial dependent dilation with advancing aging [3][4][5][6][7].This perspective will discuss new information concerning the role of increased NFκB signaling in mediating vascular endothelial dysfunction with aging in humans.
Source: Aging
Institution: University of Colorado Boulder
Language: English
Subfield: Physiology
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W1503756158