胰腺炎的发病机制和自噬的作用

IF 1.5 Q3 GASTROENTEROLOGY & HEPATOLOGY
Ioannis Tsomidis, A. Voumvouraki, E. Kouroumalis
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引用次数: 0

摘要

急性和慢性胰腺炎的发病机制近来有了新的发展,因为新的研究结果表明,胰腺炎的发病机制十分复杂,涉及多种途径。在这篇综述中,介绍了目前有证据表明多种机制共同作用诱发和延续胰腺炎的情况。由于自噬目前被认为是急性和慢性胰腺炎病理生理学的基本机制,因此讨论了自噬途径的基本原理,以便更好地理解胰腺炎的病理生理学机制。此外,还分析了发病机制的各个方面,包括胰蛋白酶原激活、ER应激和线粒体功能障碍、炎症的影响、巨噬细胞参与先天性免疫,以及胰腺星状细胞在纤维化发展中的意义。此外,还介绍了关于外泌体和 miRNA 调控作用的最新发现。最后,综述了自噬在胰腺炎的保护和加重中的作用以及可能的治疗意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Pathogenesis of Pancreatitis and the Role of Autophagy
The pathogenesis of acute and chronic pancreatitis has recently evolved as new findings demonstrate a complex mechanism operating through various pathways. In this review, the current evidence indicating that several mechanisms act in concert to induce and perpetuate pancreatitis were presented. As autophagy is now considered a fundamental mechanism in the pathophysiology of both acute and chronic pancreatitis, the fundamentals of the autophagy pathway were discussed to allow for a better understanding of the pathophysiological mechanisms of pancreatitis. The various aspects of pathogenesis, including trypsinogen activation, ER stress and mitochondrial dysfunction, the implications of inflammation, and macrophage involvement in innate immunity, as well as the significance of pancreatic stellate cells in the development of fibrosis, were also analyzed. Recent findings on exosomes and the miRNA regulatory role were also presented. Finally, the role of autophagy in the protection and aggravation of pancreatitis and possible therapeutic implications were reviewed.
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来源期刊
Gastroenterology Insights
Gastroenterology Insights GASTROENTEROLOGY & HEPATOLOGY-
CiteScore
2.80
自引率
3.40%
发文量
35
审稿时长
10 weeks
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