Angiotensin II accelerates endothelial progenitor cell senescence through induction of oxidative stress

Abstract

Ang II increases gp91phox expression in EPC, which may contribute to oxidative stress, as evidenced by peroxynitrite formation. Ang II accelerates the onset of EPC senescence via increased oxidative stress, which may be related to telomerase inactivation. In addition, Ang II-induced EPC senescence leads to the impairment of proliferative activity.

Nox enzymes, ROS, and chronic disease: An example of antagonistic pleiotropy

“…Chronic activity of Nox enzymes also inactivates telomerase and may promote senescence of endothelial progenitor cells [90]. Therefore, inhibition of Nox2 and/or Nox1 is likely to be useful for the prevention and treatment of atherosclerosis.…”

Premature vascular senescence in metabolic syndrome: Could it be prevented and reversed by a selenorganic antioxidant and peroxynitrite scavenger ebselen?

“…Decreased numbers and increased proportion of senescent EPC has been reported in patients with preeclampsia (34) or hypertension (35). Angiotensin II can induce EPC senescence through the induction of oxidative stress and influence telomerase activity (36). Oxidized low-density lipoprotein induces EPC senescence and dysfunction (37).…”

Endothelial progenitor cells relationships with clinical and biochemical factors in a human model of blunted angiotensin II signaling

“…In fact, the level of EPCs has been reported to be predictive of CV events, 4 and the loss of EPCs to have a role in the development of CV disease. Imanishi et al 5 have reported that Angiotensin II (Ang II) accelerates the onset of EPCs senescence through enhanced oxidative stress, which in turn leads to the impairment of proliferative activity in EPCs. In addition, the correction of EPCs dysfunction by treatment with Ang II type 1 receptor blockers further points to a role for Ang II and Ang II-mediated oxidative stress in EPC 6,7 as well as endothelial dysfunction.…”