Reference and Translation Centre for Cardiac Stem Cell Therapy, University of Rostock, Germany.
Can J Physiol Pharmacol. 2012 Mar;90(3):287-93. doi: 10.1139/y11-108. Epub 2012 Feb 24.
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.
血管紧张素 II 是肾素-血管紧张素系统的主要效应肽,通过其受体(包括 AT(1)和 AT(2)受体)干扰心脏重构和修复。以前被忽视的 AT(2)R 的功能相关性目前正在被深入研究。用 AT(1)R 阻滞剂进行的药物治疗改善了缺血性心脏损伤患者的预后,这可能涉及对 AT(2)R 的间接刺激。先前的实验研究清楚地表明 AT(2)R 在组织修复和再生中具有保护作用。我们最近在大鼠心脏和骨髓中鉴定出了 c-kit(+)AT(2)R(+)祖细胞群,在诱导心肌梗死后其数量增加。进一步的实验证据表明,AT(2)R 介导了 c-kit(+)祖细胞的心脏归巢和修复过程。通过 AT(1)R 阻滞剂或直接通过 AT(2)R 激动剂或两者联合刺激 AT(2)R,可能为改善源自心血管疾病患者的干细胞/祖细胞的再生潜力提供转化选择。