TGF-β1 Signaling and Tissue Fibrosis
TGF-β1 Signaling and Tissue Fibrosis
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TGF-β1信号通路与组织纤维化
DOI：
10.1101/cshperspect.a022293
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发表时间：
2018-04-01
影响因子：
7.2
通讯作者：
Chapman, Harold A.
中科院分区：
文献类型：
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作者：
Kim, Kevin K.;Sheppard, Dean;Chapman, Harold A.
tgf - β 1的激活启动了一个对许多器官的伤口修复很重要的临时胶原积累程序。然而，暂时性细胞外基质强化的结果往往演变为进行性纤维化，导致全世界的发病率和死亡率。为了避免这种适应性不良的结果，tgf - β 1信号在多个水平上受到调节，并与限制积累的反馈信号密切相关。在这里，我们研究了目前对tgf - β 1的核心功能的理解，包括促进胶原积累、促进生理修复的平行途径以及导致进行性纤维化的病理触发因素。更好地理解这些过程的隐含意义是确定需要进一步推进的治疗机会，以限制或逆转器官纤维化。
Activation of TGF-beta 1 initiates a program of temporary collagen accumulation important to wound repair in many organs. However, the outcome of temporary extracellular matrix strengthening all too frequently morphs into progressive fibrosis, contributing to morbidity and mortality worldwide. To avoid this maladaptive outcome, TGF-beta 1 signaling is regulated at numerous levels and intimately connected to feedback signals that limit accumulation. Here, we examine the current understanding of the core functions of TGF-beta 1 in promoting collagen accumulation, parallel pathways that promote physiological repair, and pathological triggers that tip the balance toward progressive fibrosis. Implicit in better understanding of these processes is the identification of therapeutic opportunities that will need to be further advanced to limit or reverse organ fibrosis.