Abstract
The identification of endothelial progenitor cells (EPCs) has led to a significant paradigm in the field of vascular biology and opened a door to the development of new therapeutic approaches. Based on the current evidence, it appears that EPCs may make both direct contribution to neovascularization and indirectly promote the angiogenic function of local endothelial cells via secretion of angiogenic factors. This concept of arterial wall repair mediated by bone marrow (BM)-derived EPCs provided an alternative to the local “response to injury hypothesis” for development of atherosclerotic inflammation. Increased oxidant stress has been proposed as a molecular mechanism for endothelial dysfunction, in part by reducing nitric oxide (NO) bioavailability. EPCs function may also be highly dependent on a well-controlled oxidant stress because EPCs NO bioavailability (which is highly sensitive to oxidant stress) is critical for their in vivo function. The critical question is whether oxidant damage directly leads to an impairment in EPCs function. It was revealed that activation of angiotensin II (Ang II) type 1 receptor stimulates nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase in the vascular endothelium and leads to production of reactive oxygen species. We observed that Ang II accelerates both BM- and peripheral blood (PB)-derived EPCs senescence by a gp91phox-mediated increase of oxidative stress, resulting in EPCs dysfunction. Consistently, both Ang II receptor 1 blockers (ARBs) and angiotensin converting enzyme (ACE) inhibitors have been reported to increase the number of EPCs in patients with cardiovascular disease. In this review, we describe current understanding of the contributions of oxidative stress in cardiovascular disease, focusing on the potential mechanisms of EPCs senescence.
Highlights
The identification of endothelial progenitor cells (EPCs) has led to a significant paradigm shift in the field of vascular biology
Recent data show that the vascular regenerative potential of patients with cardiovascular risk factors may be impaired as a consequence of reduced number and function of circulating EPCs that can support endothelial maintenance and ischemia-induced neovascularization
Recent studies have demonstrated a critical role of oxidative stress in the EPCs dysfunction
Summary
The identification of endothelial progenitor cells (EPCs) has led to a significant paradigm shift in the field of vascular biology. Based on the current evidence, it appears that EPCs may directly contribute to neovascularization and indirectly promote the angiogenic function of local endothelial cells via secretion of angiogenic factors. According to this new theory, the arterial wall can deal fairly well with multiple circulating and local. Prior studies have demonstrated that oxidative stress directly contributes to endothelial dysfunction and vascular disease [9,10,11,12] These observations suggest that EPCs, in contrast to mature endothelial cells, are uniquely equipped with antioxidant defence systems to resist ROS-driven cytotoxicity if they are active participants in various repairs in ischemic tissues. The current review describes the characterstics and properties of EPCs, focusing on the effects of oxidative stress on EPCs senescence
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