Antifibrotic therapies to control cardiac fibrosis.
Antifibrotic therapies to control cardiac fibrosis.
复制标题
抗纤维化治疗控制心脏纤维化。
DOI：
10.1186/s40824-016-0060-8
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发表时间：
2016
影响因子：
11.3
通讯作者：
Guan J
中科院分区：
文献类型：
--
作者：
Fan Z;Guan J
心肌梗死后自然发生心脏纤维化。虽然最初形成的纤维化组织防止梗死的心脏组织破裂，但心脏纤维化的进展不断扩大纤维化组织的大小并导致心脏功能下降。心脏纤维化最终使梗塞的心脏发展成心力衰竭。抑制心脏纤维化的进展对预防心力衰竭至关重要。然而，目前还没有有效的治疗方法。肌成纤维细胞是心脏纤维化的主要原因。它们通过由细胞因子如转化生长因子β（TGF-β）、血管紧张素II和血小板衍生生长因子（PDGF）驱动的心脏成纤维细胞分化、纤维细胞分化、上皮向间充质转分化和内皮向间充质转化而形成。已证明抑制肌成纤维细胞形成的方法可预防心脏纤维化，包括抗纤维化药物的全身递送、生物材料的局部递送、生物材料和抗纤维化药物的局部递送以及使用生物材料的细胞的局部递送。本文就心脏纤维化治疗的最新进展作一综述。
Cardiac fibrosis occurs naturally after myocardial infarction. While the initially formed fibrotic tissue prevents the infarcted heart tissue from rupture, the progression of cardiac fibrosis continuously expands the size of fibrotic tissue and causes cardiac function decrease. Cardiac fibrosis eventually evolves the infarcted hearts into heart failure. Inhibiting cardiac fibrosis from progressing is critical to prevent heart failure. However, there is no efficient therapeutic approach currently available. Myofibroblasts are primarily responsible for cardiac fibrosis. They are formed by cardiac fibroblast differentiation, fibrocyte differentiation, epithelial to mesenchymal transdifferentiation, and endothelial to mesenchymal transition, driven by cytokines such as transforming growth factor beta (TGF-β), angiotensin II and platelet-derived growth factor (PDGF). The approaches that inhibit myofibroblast formation have been demonstrated to prevent cardiac fibrosis, including systemic delivery of antifibrotic drugs, localized delivery of biomaterials, localized delivery of biomaterials and antifibrotic drugs, and localized delivery of cells using biomaterials. This review addresses current progresses in cardiac fibrosis therapies.