Angiotensin IV protects against angiotensin II-induced cardiac injury via AT4 receptor |
| |
| Authors: | Yang Hui Zeng Xiang-Jun Wang Hong-Xia Zhang Li-Ke Dong Xiao-Li Guo Shubin Du Jie Li Hui-Hua Tang Chao-Shu |
| |
| Affiliation: | aThe Key Laboratory of Remodeling-related Cardiovascular Diseases, Department of Pathology School of Basic Medical Sciences, Capital Medical University, Beijing 100069, China;bThe Department of Pathology and Pathophysiology, Capital Medical University, Beijing 100069, China;cThe Department of Emergency Medicine, Peking Union Medical Hospital, Beijing 100730, China;dThe Key Laboratory of Remodeling-related Cardiovascular Diseases, Beijing An Zhen Hospital, Capital Medical University, Ministry of Education, Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing 100029, China |
| |
| Abstract: | Angiotensin II (Ang II) is an important regulator of cardiac function and injury in hypertension. The novel Ang IV peptide/AT4 receptor system has been implicated in several physiological functions and has some effects opposite to those of Ang II. However, little is known about the role of this system in Ang II-induced cardiac injury. Here we studied the effect of Ang IV on Ang II-induced cardiac dysfunction and injury using isolated rat hearts, neonatal cardiomyocytes and cardiac fibroblasts. We found that Ang IV significantly improved Ang II-induced cardiac dysfunction and injury in the isolated heart in response to ischemia/reperfusion (I/R). Moreover, Ang IV inhibited Ang II-induced cardiac cell apoptosis, cardiomyocyte hypertrophy, and proliferation and collagen synthesis of cardiac fibroblasts; these effects were mediated through the AT4 receptor as confirmed by siRNA knockdown. These findings suggest that Ang IV may have a protective effect on Ang II-induced cardiac injury and dysfunction and may be a novel therapeutic target for hypertensive heart disease. |
| |
| Keywords: | Angiotensin II Angiotensin IV Cardiac function Hypertrophy Fibroblast proliferation AT4 receptor |
| 本文献已被 ScienceDirect PubMed 等数据库收录！ |
|
