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Wnt 通路相关机制调控慢性阻塞性肺疾病气道病变的进展。

Mechanistic Regulation of Wnt Pathway-Related Progression of Chronic Obstructive Pulmonary Disease Airway Lesions.

机构信息

Department of Respiratory and Critical Care Medicine, The Third Affiliated Hospital, Southern Medical University, Guangzhou, Guangdong, 510630, People's Republic of China.

出版信息

Int J Chron Obstruct Pulmon Dis. 2023 May 15;18:871-880. doi: 10.2147/COPD.S391487. eCollection 2023.

DOI:10.2147/COPD.S391487
PMID:37215745
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10198175/
Abstract

Chronic obstructive pulmonary disease (COPD) is a chronic disease associated with inflammation and structural changes in the airways and lungs, resulting from a combination of genetic and environmental factors. This interaction highlights significant genes in early life, particularly those involved in lung development, such as the Wnt signaling pathway. The Wnt signaling pathway plays an important role in cell homeostasis, and its abnormal activation can lead to the occurrence of related diseases such as asthma, COPD, and lung cancer. Due to the fact that the Wnt pathway is mechanically sensitive, abnormal activation of the Wnt pathway by mechanical stress contributes to the progression of chronic diseases. But in the context of COPD, it has received little attention. In this review, we aim to summarize the important current evidence on mechanical stress through the Wnt pathway in airway inflammation and structural changes in COPD and to provide potential targets for COPD treatment strategies.

摘要

慢性阻塞性肺疾病(COPD)是一种与气道和肺部炎症和结构改变相关的慢性疾病,是遗传和环境因素共同作用的结果。这种相互作用凸显了生命早期的重要基因,特别是那些与肺发育有关的基因,如 Wnt 信号通路。Wnt 信号通路在细胞内稳态中发挥着重要作用,其异常激活可导致相关疾病的发生,如哮喘、COPD 和肺癌。由于 Wnt 途径具有机械敏感性,机械应激引起的 Wnt 途径异常激活可促进慢性疾病的进展。但在 COPD 的背景下,这一机制尚未得到充分关注。在这篇综述中,我们旨在总结气道炎症和 COPD 结构改变中通过 Wnt 途径的机械应激的重要现有证据,并为 COPD 治疗策略提供潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0550/10198175/c524f068ebb2/COPD-18-871-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0550/10198175/c16cfd9fe208/COPD-18-871-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0550/10198175/c524f068ebb2/COPD-18-871-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0550/10198175/c16cfd9fe208/COPD-18-871-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0550/10198175/c524f068ebb2/COPD-18-871-g0002.jpg

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