Why the study?
Does AT2R stimulation improve the regenerative potential of stem/progenitor cells in cardiac repair?
Does AT2R stimulation improve the regenerative potential of stem/progenitor cells in cardiac repair?
Stimulation of the AT2 receptor may offer a translational approach to enhance stem cell-mediated cardiac repair after ischemic injury.
May support AT2R-targeted enhancement of progenitor cell repair; leaves open clinical translation in ischemic heart disease.
Angiotensin II, the main effector peptide of the renin-angiotensin system, interferes with cardiac remodeling and repair through its receptors, including AT(1) and AT(2) receptor (R). The functional relevance of the previously neglected AT(2)R is currently intensively studied. Pharmacological therapies with AT(1)R blockers have improved outcomes in patients with ischemic heart injury, probably involving an indirect stimulation of AT(2)R. Previous experimental studies have clearly shown a protective action of AT(2)R in tissue repair and regeneration. We have recently identified the c-kit(+)AT(2)R(+) progenitor cell population in rat heart and bone marrow, which increases after induction of myocardial infarction. Further experimental evidence demonstrates that AT(2)R mediates cardiac homing and repair process of the c-kit(+) progenitor cells. AT(2)R stimulation through AT(1)R blockers or directly by AT(2)R agonist or both in combination may potentially offer the translational options to improve the regenerative potentials of stem/progenitor cells derived from patients with cardiovascular disease.
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Ludwig et al. (2012) studied this question.
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