肌成纤维细胞:TGFβ-1,一种通过调节PPARγ和典型WNT通路之间的平衡在纤维化中发挥关键作用的导体

Y. Lecarpentier, O. Schussler, V. Claes, Alexandre Vallée
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引用次数: 16

摘要

肌成纤维细胞是一种非肌肉收缩性细胞,在正常妊娠期间发生在人体胎盘干绒毛等器官中。它们具有收缩和放松的能力,以响应绒毛间室体积的变化。肌成纤维细胞也存在于许多病理状态中,并参与肝、肺、肾和心脏等多个器官的伤口愈合和纤维化过程。在纤维化过程中,收缩现象是一种无松弛机制,与细胞外基质(ECM)中胶原的合成有关,这导致不可逆的纤维化、组织收缩,最终导致肌成纤维细胞凋亡。肌成纤维细胞的分子马达是非肌肌球蛋白II型(NMII)。成纤维细胞向肌成纤维细胞的分化在很大程度上受到转化生长因子-β1(TGF-β1)的调节。该系统以阳性方式调节经典的WNT/β-catenin通路,以阴性方式调节PPARγ。WNT/β-catenin促进纤维化,PPARγ预防纤维化。这篇综述的重点是肌成纤维细胞的收缩特性和调节PPARγ和经典WNT/β-catenin通路之间拮抗作用的TGF-β1导体。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Myofibroblast: TGFβ-1, A Conductor which Plays a Key Role in Fibrosis by Regulating the Balance between PPARγ and the Canonical WNT Pathway
Myofibroblasts are non-muscular contractile cells that occur physiologically in organs such as in stem villi of the human placenta during normal pregnancies. They have the ability to contract and relax in response to changes in the volume of the intervillous chamber. Myofibroblasts are also found in many pathological states, and are involved in wound healing and fibrosis processes in several organs such as liver, lung, kidney, and heart. During fibrosis, the contractile phenomenon is a relaxation-free mechanism, associated with the synthesis of collagen in the extracellular matrix (ECM), which leads to irreversible fibrosis, tissue retraction and finally apoptosis of the myofibroblasts. The molecular motor of myofibroblasts is the non-muscle myosin type II (NMII). Differentiation of fibroblasts into myofibroblast is largely regulated by the Transforming Growth Factor-β1 (TGF-β1). This system regulates the canonical WNT/β-catenin pathway in a positive manner and PPARγ in a negative manner. WNT/β-catenin promotes fibrosis while PPARγ prevents fibrosis. This review focuses on the contractile properties of myofibroblasts and on the TGF-β1 conductor which regulates the antagonism between PPARγ and the canonical WNT/β-catenin pathway.
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