Developmental signalling pathways in renal fibrosis: the roles of Notch, Wnt and Hedgehog.
Developmental signalling pathways in renal fibrosis: the roles of Notch, Wnt and Hedgehog.
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DOI：
10.1038/nrneph.2016.54
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发表时间：
2016-07
期刊：
影响因子：
--
通讯作者：
Susztak K
中科院分区：
文献类型：
--
作者：
Edeling M;Ragi G;Huang S;Pavenstädt H;Susztak K
肾纤维化是肾脏功能下降的组织学表现。纤维化是一种反应性过程，是对过度上皮损伤和炎症的反应。在这里，我们描述了三个关键的发育信号通路- notch， Wnt和hedgehog -如何在肾损伤反应中被重新激活。虽然损伤组织的修复需要这些通路的短暂激活，但它们的持续激活会促进纤维化。过量的Wnt和Notch表达抑制上皮细胞分化，而增加的Wnt和Hh表达诱导成纤维细胞增殖和肌成纤维细胞转分化。Notch、Wnt和Hedgehog是根本不同的信号机制，但它们的编排激活似乎对纤维化和胚胎肾脏发育同样重要。降低Notch、Wnt或Hh信号的活性可能是改善慢性肾脏疾病发展的一种新的治疗策略。
Kidney fibrosis is the histological manifestation of functional decline in the kidney. Fibrosis is a reactive process that develops in response to excessive epithelial injury and inflammation. Here, we describe how three key developmental signalling pathways—Notch, Wnt and Hedgehog—are reactivated in response to kidney injury. Although transient activation of these pathways is needed for repair of injured tissue, their sustained activation promotes fibrosis. Excessive Wnt and Notch expression prohibit epithelial differentiation whereas increased Wnt and Hh expression induce fibroblast proliferation and myofibroblastic transdifferentiation. Notch, Wnt and Hedgehog are fundamentally different signalling mechanisms, but their choreographed activation seems to be just as important for fibrosis as it is for embryonic kidney development. Decreasing the activity of Notch, Wnt, or Hh signalling could potentially be a new therapeutic strategy to ameliorate the development of chronic kidney disease.
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