Suppression of tissue inhibitors of metalloproteinases may reverse severe pulmonary arterial hypertension.
Suppression of tissue inhibitors of metalloproteinases may reverse severe pulmonary arterial hypertension.
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抑制金属蛋白酶的组织抑制剂可以逆转严重的肺动脉高压。
DOI：
10.3109/14653249.2010.536215
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发表时间：
2011
期刊：
影响因子：
4.5
通讯作者：
Xingxiang Wang
中科院分区：
文献类型：
--
作者：
Weiliang Tang;Hangyuan Guo;Jinxiu Yang;Bin Chen;Xingxiang Wang
肺动脉高压（PAH）是一种致死性疾病，其特征是肺血管阻力和血管重塑进行性增加，导致右心衰竭和早期死亡。PAH的病理变化与肺动脉内皮功能障碍和血管重构有关。在患病的肺动脉中，基质金属蛋白酶（MMP）和金属蛋白酶组织抑制剂（TIMP）之间的平衡被打破。在此过程中，TIMP表达上调，抑制MMP，促进细胞外基质（ECM）沉积，最终导致血管重塑。那么，如果TIMP在病变肺血管中表达下调，PAH会发生什么变化？我们推测，在PAH晚期降低TIMP可能通过改善血管重构和内皮修复来逆转重度PAH。
Pulmonary arterial hypertension (PAH) is a fatal disease characterized by a progressive increase in pulmonary vascular resistance and vascular remodeling leading to right heart failure and early death. The pathology of PAH is associated with endothelium dysfunction and vascular remodeling in pulmonary arteries. In diseased pulmonary arteries, the balance between matrix metalloproteinases (MMP) and tissue inhibitors of metalloproteinases (TIMP) is broken down. In this process, TIMP are up-regulated, which inhibits MMP, promotes extracellular matrix (ECM) deposition and finally leads to vascular remodeling. So, what would happen to PAH if the expression of TIMP was down-regulated in diseased pulmonary vessels? We hypothesize that the attenuation of TIMP at the advanced stage of PAH might reverse severe PAH, via ameliorating vascular remodeling and endothelium repair.
影响因子：
9.3
作者：
Zhao, You-Yang;Malik, Asrar B.
通讯作者：
Malik, Asrar B.
基质降解酶在大鼠肺血管重塑中的表达。
DOI：
10.1152/ajplung.1998.275.2.l398
发表时间：
1998
期刊：
The American journal of physiology
影响因子：
--
作者：
Thakker-Varia,S;Tozzi,CA;Poiani,GJ;Babiarz,JP;Tatem,L;Wilson,FJ;Riley,DJ
通讯作者：
Riley,DJ
影响因子：
5.7
作者：
Tuder, RM;Cool, CD;Voelkel, NE
通讯作者：
Voelkel, NE