Therapeutic potential of autophagy in immunity and inflammation: current and future perspectives

Author:

Zuo Hui,Chen Cheng,Sa Yalian

Abstract

AbstractAutophagy is recognized as a lysosomal degradation pathway important for cellular and organismal homeostasis. Accumulating evidence has demonstrated that autophagy is a paradoxical mechanism that regulates homeostasis and prevents stress under physiological and pathological conditions. Nevertheless, how autophagy is implicated in immune responses remains unclear. It is well established that autophagy bridges innate and adaptive immunity, while autophagic dysfunction is closely related to infection, inflammation, neurodegeneration, and tumorigenesis. Therefore, autophagy has attracted great attention from fundamental and translational fields due to its crucial role in inflammation and immunity. Inflammation is involved in the development and progression of various human diseases, and as a result, autophagy might be a potential target to prevent and treat inflammatory diseases. Nevertheless, insufficient autophagy might cause cell death, perpetrate inflammation, and trigger hereditary unsteadiness. Hence, targeting autophagy is a promising disease prevention and treatment strategy. To accomplish this safely, we should thoroughly understand the basic aspects of how autophagy works. Herein, we systematically summarized the correlation between autophagy and inflammation and its implication for human diseases.

Funder

National Science Funding of China

Publisher

Springer Science and Business Media LLC

Subject

Pharmacology,General Medicine

Cited by 3 articles. 订阅此论文施引文献 订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献

同舟云学术

1.学者识别学者识别

2.学术分析学术分析

3.人才评估人才评估

"同舟云学术"是以全球学者为主线,采集、加工和组织学术论文而形成的新型学术文献查询和分析系统,可以对全球学者进行文献检索和人才价值评估。用户可以通过关注某些学科领域的顶尖人物而持续追踪该领域的学科进展和研究前沿。经过近期的数据扩容,当前同舟云学术共收录了国内外主流学术期刊6万余种,收集的期刊论文及会议论文总量共计约1.5亿篇,并以每天添加12000余篇中外论文的速度递增。我们也可以为用户提供个性化、定制化的学者数据。欢迎来电咨询!咨询电话:010-8811{复制后删除}0370

www.globalauthorid.com

TOP

Copyright © 2019-2024 北京同舟云网络信息技术有限公司
京公网安备11010802033243号  京ICP备18003416号-3