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热休克家族在溃疡性结肠炎中的研究进展

Advances of Heat Shock Family in Ulcerative Colitis.

作者信息

Gong Min, Zhang Fengrui, Miao Yinglei, Niu Junkun

机构信息

Department of Gastroenterology, The First Affiliated Hospital of Kunming Medical University, Kunming, China.

Yunnan Province Clinical Research Center for Digestive Diseases, Kunming, China.

出版信息

Front Pharmacol. 2022 May 12;13:869930. doi: 10.3389/fphar.2022.869930. eCollection 2022.

DOI:10.3389/fphar.2022.869930
PMID:35645809
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9133716/
Abstract

Ulcerative Colitis (UC) is a non-specific and chronic inflammatory disease of colonic mucosa whose exact etiology and mechanisms remain unclear. The incidence rate of UC is increasing year by year worldwide. What followed is that the medical costs are also rising rapidly. Therefore, it is urgent to understand the pathogenesis and find promising therapeutic targets for UC. Intestinal mucosal homeostasis is essential for normal bowel function, and its imbalance may be an important pathogenesis of UC. Endogenous homeostatic regulators play roles in repairing intestinal mucosa injury after stress. Heat shock family proteins are essential endogenous homeostasis factors. They can inhibit inflammation, regulate intestinal epithelial cells' survival and death, and promote mucosal healing. Thus, they play important roles in sustaining intestinal mucosal homeostasis and protecting against UC progression. However, the heat shock family may promote UC carcinogenesis. Here, we summarize the advances in the research of the functions of the heat shock family in UC. And this review is an attempt to light on the etiopathogenesis of UC, highlighting the endogenous protective mechanisms, hoping to provide a novel therapeutic target for UC treatment.

摘要

溃疡性结肠炎(UC)是一种结肠黏膜的非特异性慢性炎症性疾病,其确切病因和发病机制尚不清楚。全球范围内,UC的发病率逐年上升。随之而来的是医疗费用也在迅速增加。因此,迫切需要了解UC的发病机制并找到有前景的治疗靶点。肠道黏膜稳态对于正常肠道功能至关重要,其失衡可能是UC的重要发病机制。内源性稳态调节因子在应激后修复肠道黏膜损伤中发挥作用。热休克家族蛋白是重要的内源性稳态因子。它们可以抑制炎症,调节肠道上皮细胞的存活和死亡,并促进黏膜愈合。因此,它们在维持肠道黏膜稳态和防止UC进展中发挥重要作用。然而,热休克家族可能促进UC癌变。在此,我们总结热休克家族在UC中功能的研究进展。本综述旨在阐明UC的病因发病机制,突出内源性保护机制,希望为UC治疗提供新的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f16d/9133716/ad2cd90d70b9/fphar-13-869930-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f16d/9133716/a6acfadff1aa/fphar-13-869930-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f16d/9133716/ad2cd90d70b9/fphar-13-869930-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f16d/9133716/a6acfadff1aa/fphar-13-869930-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f16d/9133716/ad2cd90d70b9/fphar-13-869930-g002.jpg

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