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自噬与气道纤维化:存在关联吗?

Autophagy and airway fibrosis: Is there a link?

作者信息

Kota Anudeep, Deshpande Deepak A, Haghi Mehra, Oliver Brian, Sharma Pawan

机构信息

Faculty of Science, University of Technology Sydney, Sydney, NSW, 2007, Australia.

Woolcock Emphysema Centre, Woolcock Institute of Medical Research, The University of Sydney, Sydney, NSW, 2037, Australia.

出版信息

F1000Res. 2017 Apr 3;6:409. doi: 10.12688/f1000research.11236.2. eCollection 2017.

DOI:10.12688/f1000research.11236.2
PMID:28815017
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5416906/
Abstract

In the past decade, an emerging process named "autophagy" has generated intense interest in many chronic lung diseases. Tissue remodeling and fibrosis is a common feature of many airway diseases, and current therapies do not prevent or reverse these structural changes. Autophagy has evolved as a conserved process for bulk degradation and recycling of cytoplasmic components to maintain basal cellular homeostasis and healthy organelle populations in the cell. Furthermore, autophagy serves as a cell survival mechanism and can also be induced by chemical and physical stress to the cell. Accumulating evidence demonstrates that autophagy plays an essential role in vital cellular processes, including tissue remodeling. This review will discuss some of the recent advancements made in understanding the role of this fundamental process in airway fibrosis with emphasis on airway remodeling, and how autophagy can be exploited as a target for airway remodeling in asthma and chronic obstructive pulmonary disease.

摘要

在过去十年中,一个名为“自噬”的新兴过程引发了人们对许多慢性肺病的浓厚兴趣。组织重塑和纤维化是许多气道疾病的共同特征,而目前的治疗方法无法预防或逆转这些结构变化。自噬已演变成一种保守的过程,用于大量降解和循环利用细胞质成分,以维持细胞的基础内环境稳定和健康的细胞器群体。此外,自噬作为一种细胞存活机制,也可由细胞受到的化学和物理应激诱导产生。越来越多的证据表明,自噬在包括组织重塑在内的重要细胞过程中发挥着至关重要的作用。本综述将讨论在理解这一基本过程在气道纤维化中的作用方面取得的一些最新进展,重点是气道重塑,以及自噬如何能够被用作哮喘和慢性阻塞性肺疾病气道重塑的一个靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f32c/5998013/d082d310b3ae/f1000research-6-15658-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f32c/5998013/c68ee8ee6027/f1000research-6-15658-g0000.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f32c/5998013/d082d310b3ae/f1000research-6-15658-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f32c/5998013/c68ee8ee6027/f1000research-6-15658-g0000.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f32c/5998013/d082d310b3ae/f1000research-6-15658-g0001.jpg

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