J Clin Invest. 2011 Aug;121(8):2975-7. doi: 10.1172/JCI58389. Epub 2011 Jul 25.
Each normal heart beat is triggered by an electrical impulse emitted from a group of specialized cardiomyocytes that together form the sinoatrial node (SAN). In this issue of the JCI, Swaminathan and colleagues demonstrate a new molecular mechanism that can disrupt the normal beating of the heart: angiotensin II - typically found in increased levels in heart failure and hypertension - oxidizes and activates Ca2+/calmodulin-dependent kinase II via NADPH oxidase activation, causing SAN cell death. The loss of SAN cells produces an electrical imbalance termed the "source-sink mismatch," which may contribute to the SAN dysfunction that affects millions of people later in life and complicates a number of heart diseases.
每一次正常的心跳都是由一组特殊的心肌细胞发出的电脉冲触发的，这些细胞共同构成了窦房结（SAN）。在本期 JCI 中，Swaminathan 及其同事展示了一种新的分子机制，这种机制可以破坏心脏的正常跳动：血管紧张素 II - 通常在心力衰竭和高血压中发现水平升高 - 通过 NADPH 氧化酶的激活使钙/钙调蛋白依赖性激酶 II 氧化和激活，导致 SAN 细胞死亡。SAN 细胞的丧失会产生一种称为“源-汇不匹配”的电不平衡，这可能导致 SAN 功能障碍，影响数以百万计的人在以后的生活中，并使许多心脏病复杂化。
