Department of Nephrology, The First Hospital of Jilin University, 71 XinMin Street, Changchun, Jilin, China.
Int Urol Nephrol. 2020 Jul;52(7):1287-1295. doi: 10.1007/s11255-020-02474-2. Epub 2020 May 6.
Renal fibrosis is the most common pathological manifestation of chronic kidney disease (CKD), and with numerous influencing factors, its pathogenesis is complex. Epithelial-mesenchymal transition (EMT) is known to promote the progression of renal fibrosis via alterations in the secreted proteome. Moreover, blocking or even reversing EMT can effectively reduce the degree of fibrosis. As such, targeting the key molecules responsible for promoting EMT may be an effective strategy for inhibiting renal fibrosis. Research in recent years has demonstrated that hypoxia-inducible factor 1α (HIF-1α) acts to promote renal fibrosis through regulation of EMT. However, the relationship between HIF-1α and EMT remains incompletely understood. In the present review, the underlying mechanism of the interaction between HIF-1α and EMT is explored to provide novel insight into the pathogenesis of renal fibrosis and new ideas for early targeted intervention.
肾纤维化是慢性肾脏病(CKD)最常见的病理表现,其发病机制复杂,受多种影响因素的影响。上皮-间充质转化(EMT)通过改变分泌的蛋白质组来促进肾纤维化的进展。此外,阻断甚至逆转 EMT 可以有效降低纤维化程度。因此,针对促进 EMT 的关键分子可能是抑制肾纤维化的有效策略。近年来的研究表明,缺氧诱导因子 1α(HIF-1α)通过调节 EMT 促进肾纤维化。然而,HIF-1α 与 EMT 之间的关系尚不完全清楚。本综述探讨了 HIF-1α 与 EMT 相互作用的潜在机制,为肾纤维化的发病机制提供了新的认识,并为早期靶向干预提供了新的思路。