Targeting ACE2/Angiotensin-(1-7)/Mas Receptor Axis in the Vascular Progenitor Cells for Cardiovascular Diseases.
2020
Bone marrow-derived hematopoietic stem/progenitor cells are vasculogenic, and play an important role in endothelial health and vascular homeostasis by participating in post-natal vasculogenesis. Progenitor cells are mobilized from bone marrow niches in response to remote ischemic injury and migrate to the areas of damage and stimulate revascularization largely by paracrine activation of angiogenic functions in the peri-ischemic vasculature. This innate vasoprotective mechanism is impaired in certain chronic clinical conditions, which leads to the development of cardiovascular complications. Members of renin angiotensin system (RAS), angiotensin converting enzymes (ACEs), ACE and ACE2, angiotensin II (Ang II), Ang-(1-7), and receptors AT1 and Mas are expressed in vasculogenic progenitor cells derived from humans and rodents. Ang-(1-7), generated by ACE2, is known to produce cardiovascular protective effects by acting on Mas receptor and is considered as a counter-regulatory mechanism to the detrimental effects of Ang II. Evidence has now been accumulating in support of the activation of ACE2/Ang-(1-7)/Mas receptor pathway by pharmacological or molecular maneuvers, stimulates mobilization of progenitor cells from bone marrow, migration to areas of vascular damage and revascularization of ischemic areas in pathological conditions. This mini-review summarizes recent studies that have enhanced our understanding of the physiology and pharmacology of vasoprotective axis in bone marrow-derived progenitor cells in health and disease. SIGNIFICANCE STATEMENT: Hematopoietic stem/progenitor cells (HSPCs) stimulate revascularization of ischemic areas. However the reparative potential is diminished in certain chronic clinical conditions leading to the development of cardiovascular diseases. ACE2 and Mas receptor are key members of the alternative axis of renin angiotensin system and are expressed in HSPCs. Accumulating evidence points to activation of ACE2 or Mas receptor as a promising approaches for restoring the reparative potential thereby to prevent the development of ischemic vascular diseases.
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