University Paris Diderot-CNRS EAC 4413, Unit of Functional and Adaptive Biology (BFA), Paris, France; Laboratory of Biochemistry and Extracellular Matrix Remodeling, BCM.FSB.USTHB, Algiers, Algeria.
University Paris Diderot-CNRS EAC 4413, Unit of Functional and Adaptive Biology (BFA), Paris, France.
Int J Cardiol. 2010 Nov 19;145(2):306-307. doi: 10.1016/j.ijcard.2009.10.043. Epub 2009 Nov 10.
Cardiac hypertrophy has been demonstrated in rat models of hyperhomocysteinemia, a major risk factor for chronic heart failure. As one of the molecular pathway which leads to cardiac hypertrophy is mediated by the serine-threonine kinase DYRK1A, we have determined the expression of Dyrk1a in the heart of hyperhomocysteinemic rats and found that hyperhomocysteinemia in rats not only induced ventricular cardiomyocyte hypertrophy but also decreased protein Dyrk1a expression. The decreased expression of Dyrk1a could be consistent with decreased antihypertrophic effects of Dyrk1a leading to cardiomyocyte hypertrophy in case of hyperhomocysteinemia.
高同型半胱氨酸血症是慢性心力衰竭的一个主要危险因素，在高同型半胱氨酸血症的大鼠模型中已经证实存在心肌肥厚。丝氨酸-苏氨酸激酶 DYRK1A 介导的一条导致心肌肥厚的分子途径，我们已经确定了 Dyrk1a 在高同型半胱氨酸血症大鼠心脏中的表达，发现高同型半胱氨酸血症不仅诱导心室肌细胞肥大，而且还降低了蛋白 Dyrk1a 的表达。Dyrk1a 表达降低可能与 Dyrk1a 的抗肥厚作用降低一致，导致高同型半胱氨酸血症时的心肌细胞肥大。
