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哺乳动物心室肌组织中存在β3肾上腺素受体(β3AR),与β1AR、β2AR结构和功能不同,β3AR主要通过抑制性G蛋白(Gi)-内皮型一氧化氮合酶(eNOS)-环磷酸鸟苷(cGMP)-蛋白激酶G(PKG)通路介导心肌的负性肌力作用。心力衰竭时,β3AR信号转导通路的各个环节都发生改变,参与调节心肌舒张收缩功能、心室重塑和细胞凋亡等病理生理学变化。
The structure and function of β1AR and β2AR are different from those of β1AR and β2AR in the mammalian ventricular myocytes. Β3AR is mainly produced by the inhibitory G protein (Gi) -endothelial nitric oxide synthase (eNOS) Glycoside (cGMP) - Protein Kinase G (PKG) Pathway Mediates Negative Intrinsic Muscle. Heart failure, β3AR signal transduction pathway changes in all aspects involved in the regulation of cardiac diastolic function, ventricular remodeling and apoptosis and other pathophysiological changes.