p38丝裂原活化蛋白激酶在β₂肾上腺素能受体诱导的心肌病中的作用：问题的核心？

Role of p38MAPK in beta(2)AR-induced cardiomyopathy: at the heart of the matter?

作者信息

Sucharov Carmen C

机构信息

University of Colorado Denver & Health Sciences Center, 4200 E Ninth Ave, Denver, CO 80262, USA.

出版信息

Future Cardiol. 2007 Jul;3(4):387-9. doi: 10.2217/14796678.3.4.387.

DOI:10.2217/14796678.3.4.387

PMID:19804229

Abstract

Peter PS, Brady JE, Yan L et al.: Inhibition of p38alpha MAPK rescues cardiomyopathy induced by overexpressed beta(2)-adrenergic receptor, but not beta(1)-adrenergic receptor. J. Clin. Invest. 117(5), 1335-1343 (2007). The role of p38MAPK in the progression of heart failure is controversial. In the reference paper, Peter and colleagues demonstrated that p38MAPK plays an important role in the progression of heart failure in transgenic mice over-expressing the beta(2) adrenergic receptor. The authors show that p38MAPK is involved in apoptosis, fibrosis and decreased left ventricle fractional shortening in mice overexpressing beta(2) adrenergic receptor but not beta(1) adrenergic receptor. These results showed that beta(1) and beta(2) adrenergic receptors induce cardiomyopathies through different signaling pathways, and suggest an important role for p38MAPK in the development of cardiac disease.

摘要

彼得·P·S、布雷迪·J·E、严·L等：抑制p38α丝裂原活化蛋白激酶可挽救由过度表达的β₂-肾上腺素能受体而非β₁-肾上腺素能受体诱导的心肌病。《临床研究杂志》117(5)，1335 - 1343(2007)。p38丝裂原活化蛋白激酶在心力衰竭进展中的作用存在争议。在参考文献中，彼得及其同事证明p38丝裂原活化蛋白激酶在过度表达β₂-肾上腺素能受体的转基因小鼠心力衰竭进展中起重要作用。作者表明，p38丝裂原活化蛋白激酶参与过度表达β₂-肾上腺素能受体而非β₁-肾上腺素能受体的小鼠的细胞凋亡、纤维化及左心室缩短分数降低。这些结果表明，β₁和β₂-肾上腺素能受体通过不同信号通路诱导心肌病，并提示p38丝裂原活化蛋白激酶在心脏疾病发展中起重要作用。