Angiotensin II induces inflammation leading to cardiac remodeling
Angiotensin II induces inflammation leading to cardiac remodeling
复制标题
血管紧张素 II 诱导炎症导致心脏重塑
DOI：
10.2741/3923
复制
发表时间：
2012-01-01
影响因子：
3.1
通讯作者：
Du, Jie
中科院分区：
文献类型：
--
作者：
Jia, Lixin;Li, Yulin;Du, Jie
高血压，尤其是肾素-血管紧张素II(Ang II)升高，会导致心脏纤维化和重构。Ang II通过其受体发挥作用，引起血流动力学和非血流动力学效应。这些效应会引发一系列炎症反应。最近的研究表明，高血压刺激白细胞向心脏的渗透，巨噬细胞、T细胞和单核细胞成纤维细胞前体细胞之间的相互作用调节促炎和抗炎因子的失衡。一些研究表明，高血压心脏的炎性微环境促进了白细胞的前馈渗透、单核细胞的分化和肌成纤维细胞的形成。肌成纤维细胞是产生细胞外基质的主要来源，其数量的增加导致胶原沉积和心脏重塑。深入了解高血压心脏重构的病理过程有助于预防和治疗高血压。
Hypertension, especially for elevated renin-angiotensin II (Ang II), induces cardiac fibrosis and remodeling. Ang II, acting via its receptors, causes both hemodynamic and nonhemodynamic effects. These effects trigger a series of inflammatory responses. Recent studies have demonstrated that hypertension stimulates infiltration of leukocytes into heart, and interaction among macrophages, T cells, and monocytic fibroblast precursor cells regulates the imbalance of pro-inflammatory and anti-inflammatory factors. Several studies have demonstrated that the inflammatory microenvironment in hypertensive heart promotes a forward feedback infiltration of leukocytes, differentiation of monocytes, and formation of myofibroblasts. An increased number of myofibroblasts, the dominant source of extracellular matrix production, results in deposition of collagen and cardiac remodeling. A thorough understanding of the pathological process underlying hypertension-induced cardiac remodeling may help in prevention and treatment.