Endothelial progenitor cells dysfunction and senescence: contribution to oxidative stress

Area of Science:

• Vascular Biology
• Cardiovascular Research
• Cellular Aging

Background:

• Endothelial progenitor cells (EPCs) are crucial for vascular repair and neovascularization.
• Oxidative stress is implicated in endothelial dysfunction and cardiovascular disease.
• The role of oxidant stress in EPCs function and senescence is not fully understood.

Purpose of the Study:

• To investigate the impact of oxidative stress on EPCs function and senescence.
• To elucidate the mechanisms by which angiotensin II (Ang II) affects EPCs.
• To explore the link between Ang II, oxidative stress, and EPCs dysfunction in cardiovascular disease.

Main Methods:

• Review of current literature on EPCs, oxidative stress, and cardiovascular disease.
• Analysis of mechanisms involving angiotensin II type 1 receptor, NADPH oxidase, and reactive oxygen species.
• Examination of EPCs senescence and dysfunction induced by Ang II.

Main Results:

• Angiotensin II accelerates senescence of bone marrow (BM)- and peripheral blood (PB)-derived EPCs.
• This acceleration is mediated by gp91phox-dependent oxidative stress, leading to EPCs dysfunction.
• EPCs function is highly sensitive to oxidant stress, impacting nitric oxide (NO) bioavailability.

Conclusions:

• Oxidative stress, particularly via Ang II, directly impairs EPCs function and promotes senescence.
• This dysfunction contributes to the pathogenesis of cardiovascular diseases.
• Therapeutic strategies targeting Ang II signaling may preserve EPCs function in cardiovascular disease patients.