Cardiac Expression of Factor X Mediates Cardiac Hypertrophy and Fibrosis in Pressure Overload (Retracted article. See vol. 7, pg. 970, 2022)
Cardiac Expression of Factor X Mediates Cardiac Hypertrophy and Fibrosis in Pressure Overload (Retracted article. See vol. 7, pg. 970, 2022)
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DOI：
10.1016/j.jacbts.2019.10.006
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发表时间：
2020-01-01
影响因子：
9.7
通讯作者：
Sabri, Abdelkarim
中科院分区：
文献类型：
--
作者：
Guo, Xinji;Kolpakov, Mikhail A.;Sabri, Abdelkarim
活化因子X是凝血级联反应的关键成分，但它是否直接调节病理性心脏重塑尚不清楚。在压力超负荷应激的小鼠中，心脏因子X mRNA表达和活性增加，同时伴有心脏肥大、纤维化、炎症和舒张功能障碍，并且反应被低凝非依赖性剂量的利伐沙班阻断。在体外，神经激素应激增加激活因子X在心肌细胞和成纤维细胞的表达，导致激活因子X介导的激活蛋白酶激活受体和促肥大和纤维化反应，分别。因此，抑制心脏表达的活化因子X可以为预防高血压患者的不良心脏重构提供有效的治疗。(C)2020年，任作家。由爱思唯尔代表美国心脏病学会基金会出版。
Activated factor X is a key component of the coagulation cascade, but whether it directly regulates pathological cardiac remodeling is unclear. In mice subjected to pressure overload stress, cardiac factor X mRNA expression and activity increased concurrently with cardiac hypertrophy, fibrosis, inflammation and diastolic dysfunction, and responses blocked with a low coagulation-independent dose of rivaroxaban. In vitro, neurohormone stressors increased activated factor X expression in both cardiac myocytes and fibroblasts, resulting in activated factor Xmediated activation of protease-activated receptors and pro-hypertrophic and -fibrotic responses, respectively. Thus, inhibition of cardiac-expressed activated factor X could provide an effective therapy for the prevention of adverse cardiac remodeling in hypertensive patients. (C) 2020 The Authors. Published by Elsevier on behalf of the American College of Cardiology Foundation.