Inhibition of matrix metalloproteinase activity by TIMP-1 gene transfer effectively treats ischemic cardiomyopathy
Inhibition of matrix metalloproteinase activity by TIMP-1 gene transfer effectively treats ischemic cardiomyopathy
复制标题
DOI：
10.1161/01.cir.0000138946.29375.49
复制
发表时间：
2004-09-14
期刊：
影响因子：
37.8
通讯作者：
Sweeney, HL
中科院分区：
文献类型：
--
作者：
Jayasankar, V;Woo, YJ;Sweeney, HL
背景-在动物模型和人类患者中，基质金属蛋白酶(MMPs)活性增强与细胞外基质降解和缺血性心力衰竭有关。方法与结果：结扎大鼠冠状动脉左前降支，心肌内直接注射携带TIMP-1基因的复制缺陷型腺病毒(n=8)或空病毒(n=8)作为对照载体，6周后取材。与对照组相比，TIMP-1组的收缩和舒张期心功能均得到显著保护(最大左心室[LV]压：TIMP-1 70+/-10对对照组56+/-12 mm Hg，P
Background-Enhanced activity of matrix metalloproteinases (MMPs) has been associated with extracellular matrix degradation and ischemic heart failure in animal models and human patients. This study evaluated the effects of MNIP inhibition by gene transfer of TIMP-1 in a rat model of ischemic cardiomyopathy.Methods and Results-Rats underwent ligation of the left anterior descending coronary artery with direct intramyocardial injection of replication-deficient adenovirus encoding TIMP-1 (n=8) or null virus as control vector (n=8), and animals were analyzed after 6 weeks. Both systolic and diastolic cardiac function was significantly preserved in the TIMP-1 group compared with control animals (maximum left ventricular [LV] pressure: TIMP-1 70+/-10 versus control 56+/-12 mmHg, P