炎症性肠病中的自噬和细胞凋亡

E. Kouroumalis, Ioannis Tsomidis, A. Voumvouraki
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摘要

炎症性肠病(IBD)的发病机制涉及多个相互关联的因素。免疫和外部因素相互影响,大多数方面仍在研究之中。自噬和细胞凋亡是决定肠粘膜单个细胞命运的两个关键途径。实验和临床数据表明,自噬和凋亡密切相关,通常相互排斥。然而,尽管关于它们作用的信息很多,但近年来转化为治疗应用的却非常有限。本综述将介绍有关这两种途径的研究。在概述了自噬和细胞凋亡之后,讨论了它们与 IBD 的关联,包括重要的有丝分裂和铁凋亡。此外,还讨论了自噬和凋亡相关基因的影响。最后,介绍了自噬和细胞凋亡在 IBD 中的相互作用,并探讨了自噬和细胞凋亡对治疗应用的影响。研究表明,自噬失调会导致肠细胞凋亡增加,并损害肠道保护屏障的紧密连接蛋白。自噬失调还会诱导溶菌酶和其他抗微生物蛋白产量的下调。由于自噬缺陷和细胞凋亡增加,鹅口疮细胞分泌的粘液也会减少。
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Autophagy and Apoptosis in Inflammatory Bowel Disease
The pathogenesis of inflammatory bowel disease (IBD) implicates several interconnecting factors. Immunity and external factors interact, and most aspects are still under investigation. Autophagy and apoptosis are two critical pathways that decide the fate of the individual cells of the intestinal mucosa. Experimental and clinical data indicate that the two are closely interconnected and usually mutually exclusive. However, despite the abundant information on their role, very limited translation into therapeutic application has been seen during recent years. In this review, research on these two pathways is presented. After a general overview of autophagy and apoptosis, their association with IBD, including the important mitophagy and ferroptosis, is discussed. The influence of autophagy- and apoptosis-related genes is also discussed. Finally, the interplay of autophagy and apoptosis in IBD is presented and the implications for treatment applications are examined. It is shown that dysregulated autophagy leads to increased apoptosis of enterocytes and impairs the tight junction proteins of the protective intestinal barrier. Dysregulated autophagy also induces the downregulation of lysozyme and the other antimicrobial proteins’ production. Mucus production by the goblet cells is also reduced due to defective autophagy and increased apoptosis.
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