French National Institute of Health and Medical Research (INSERM), UMR_S1155, Remodeling and Repair of Renal Tissue, Hôpital Tenon, Paris, France.
Sorbonne Universités, UPMC Paris 06, UMR S_1155, Paris, France.
Nephrol Dial Transplant. 2017 Feb 1;32(2):224-233. doi: 10.1093/ndt/gfw333.
Snail family zinc finger 1 (SNAI1) is a transcription factor expressed during renal embryogenesis, and re-expressed in various settings of acute kidney injury (AKI). Subjected to tight regulation, SNAI1 controls major biological processes responsible for renal fibrogenesis, including mesenchymal reprogramming of tubular epithelial cells, shutdown of fatty acid metabolism, cell cycle arrest and inflammation of the microenvironment surrounding tubular epithelial cells. The present review describes in detail the interactions of SNAI1 with AKI-associated signalling pathways. We also discuss how this central factor has been iteratively (and promisingly) targeted in a number of animal models in order to prevent or slow down renal fibrogenesis.
蜗牛家族锌指蛋白 1（SNAI1）是一种在肾胚胎发生过程中表达的转录因子，在各种急性肾损伤（AKI）情况下重新表达。SNAI1 受到严格调控，控制着导致肾纤维化的主要生物学过程，包括肾小管上皮细胞的间充质重编程、脂肪酸代谢关闭、细胞周期停滞和肾小管上皮细胞周围微环境的炎症。本综述详细描述了 SNAI1 与 AKI 相关信号通路的相互作用。我们还讨论了如何在一些动物模型中反复（并很有希望地）针对这个核心因子进行靶向治疗，以预防或减缓肾纤维化。
