人类心房纤维性颤动变化的分子机制

Molecular Mechanism of Remodeling in Human Atrial Fibrillation

近年来确认了心房纤维性颤动(AF)以促进心房的发生和维持的方式修饰了心房的电特征.并确立了节律紊乱发生的电生理变化.主要描述了功能的快变化和蛋白质表达的慢变化的分子机制,这种慢变化会引起心房纤维性颤动的电改变和收缩异常.心房纤维性颤动的一个重要分子特征是L型钙离子通道功能和蛋白质表达的减少.这种减少可能有助于保护细胞抵制由于心房纤维性颤动的激活率增加产生的潜在致死钙离子超载.对蛋白水解系统的可能作用也进行了讨论,其中重点讨论了钙蛋白酶作为一种与钙离子超载导致蛋白表达减少相联系的机制.

An important acknowledgement of the last several years is that atrial fibrillation(AF) modifies the electrical properties of the atrium in a way that promoted its occurrence and maintenance .This arrhythmogenic eletrophysiological remodeling is well established. It describes molecular changes involving rapiding functional alteration and slower changes in protein expression that cause electrical remodeling and contractile dysfunction in AF. An important molecular feature of AF is the reduction in Ltype Ca2+ channel function and protein expression .This reduction may serve to protect the cell against a potentially lethal Ca2+ overload resulting from the increased activation rate in AF. The possible role of proteolytic systems are discussed,notably the calpains as a mechanism linking Ca2+ overload to reduce protein expression.