Cardiac fibrosis: Myofibroblast-mediated pathological regulation and drug delivery strategies.
Cardiac fibrosis: Myofibroblast-mediated pathological regulation and drug delivery strategies.
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心脏纤维化：肌成纤维细胞介导的病理调节和药物输送策略。
DOI：
10.1016/j.addr.2021.03.021
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发表时间：
2021-06
影响因子：
16.1
通讯作者：
Cheng K
中科院分区：
文献类型：
--
作者：
Liu M;López de Juan Abad B;Cheng K
心脏纤维化是心脏疾病中尚未解决的问题。在初始损伤后，心脏成纤维细胞（CFs）被激活并随后分化为肌成纤维细胞（myoFbs），肌成纤维细胞是病理重塑的主要中介细胞。MyoFbs表现出增殖和分泌特性，并有助于细胞外基质（ECM）的周转和胶原沉积。肌ofbs的持续功能导致纤维化疤痕和心功能障碍。抗纤维化治疗受到纤维化机制难以捉摸和myoFbs缺乏特异性靶点的阻碍。在这篇综述中，我们将概述心脏纤维化的进展及其对心力衰竭的贡献。我们还将阐明myoFbs在调节不良重塑中的作用。myoFbs与其他参与心脏损伤和修复的细胞之间的通讯将被详细讨论。然后，将总结最近开发的治疗纤维化的治疗策略，如i)嵌合抗原受体T细胞（CAR-T）治疗与myoFbs的最佳靶点，ii)直接从干细胞重编程到静止的CFs， iii)“脱靶”小分子药物。此外，还将讨论纳米/微技术在细胞仿生平台和“多效”给药系统构建中的应用。
Cardiac fibrosis remains an unresolved problem in heart diseases. After initial injury, cardiac fibroblasts (CFs) are activated and subsequently differentiate into myofibroblasts (myoFbs) that are major mediator cells in the pathological remodeling. MyoFbs exhibit proliferative and secretive characteristics, and contribute to extracellular matrix (ECM) turnover, collagen deposition. The persistent functions of myoFbs lead to fibrotic scars and cardiac dysfunction. The anti-fibrotic treatment is hindered by the elusive mechanism of fibrosis and lack of specific targets on myoFbs. In this review, we will outline the progress of cardiac fibrosis and its contributions to the heart failure. We will also shed light on the role of myoFbs in the regulation of adverse remodeling. The communication between myoFbs and other cells that are involved in the heart injury and repair respectively will be reviewed in detail. Then, recently developed therapeutic strategies to treat fibrosis will be summarized such as i) chimeric antigen receptor T cell (CAR-T) therapy with an optimal target on myoFbs, ii) direct reprogramming from stem cells to quiescent CFs, iii) “off-target” small molecular drugs. The application of nano/micro technology will be discussed as well, which is involved in the construction of cell-based biomimic platforms and “pleiotropic” drug delivery systems.
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影响因子：
3.4
作者：
Crawford, Jeffrey R.;Haudek, Sandra B.;Cieslik, Katarzyna A.;Trial, JoAnn;Entman, Mark L.
通讯作者：
Entman, Mark L.
DOI：
10.1016/j.trsl.2014.05.001
发表时间：
2014-10
期刊：
Translational research : the journal of laboratory and clinical medicine
影响因子：
--
作者：
Cavalera M;Wang J;Frangogiannis NG
通讯作者：
Frangogiannis NG
DOI：
10.1152/ajpheart.00341.2006
发表时间：
2006-10-01
影响因子：
4.8
作者：
Chen, Jiawei;Mehta, Jawahar L.
通讯作者：
Mehta, Jawahar L.
影响因子：
6
作者：
Chambers, RC;Leoni, P;Heller, RA
通讯作者：
Heller, RA
影响因子：
56.9
作者：
Cao, Nan;Huang, Yu;Ding, Sheng
通讯作者：
Ding, Sheng