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JNK信号通路在器官纤维化中的作用。

The role of JNK signaling pathway in organ fibrosis.

作者信息

Hao Min, Lu Yandan, Yao Zhouhui, Wang Pingping, Chen Ziyan, Zhou Licheng, Yang Qiao, Sang Xianan, Wang Kuilong, Cao Gang

机构信息

School of Pharmaceutical Sciences, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310053, China; Songyang Research Institute of Zhejiang Chinese Medical University, Songyang, 323400, China.

School of Pharmaceutical Sciences, The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, 310053, China.

出版信息

J Adv Res. 2025 Aug;74:207-223. doi: 10.1016/j.jare.2024.09.029. Epub 2024 Oct 2.

DOI:10.1016/j.jare.2024.09.029
PMID:39366483
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12302471/
Abstract

BACKGROUND

Fibrosis is a tissue damage repair response caused by multiple pathogenic factors which could occur in almost every apparatus and leading to the tissue structure damage, physiological abnormality, and even organ failure until death. Up to now, there is still no specific drugs or strategies can effectively block or changeover tissue fibrosis. JNKs, a subset of mitogen-activated protein kinases (MAPK), have been reported that participates in various biological processes, such as genetic expression, DNA damage, and cell activation/proliferation/death pathways. Increasing studies indicated that abnormal regulation of JNK signal pathway has strongly associated with tissue fibrosis.

AIM OF REVIEW

This review designed to sum up the molecular mechanism progresses in the role of JNK signal pathway in organ fibrosis, hoping to provide a novel therapy strategy to tackle tissue fibrosis.

KEY SCIENTIFIC CONCEPTS OF REVIEW

Recent evidence shows that JNK signaling pathway could modulates inflammation, immunoreaction, oxidative stress and Multiple cell biological functions in organ fibrosis. Therefore, targeting the JNK pathway may be a useful strategy in cure fibrosis.

摘要

背景

纤维化是由多种致病因素引起的组织损伤修复反应,几乎可发生于每个器官,导致组织结构破坏、生理异常,甚至器官衰竭直至死亡。到目前为止,仍然没有特效药物或策略能够有效阻断或逆转组织纤维化。JNKs是丝裂原活化蛋白激酶(MAPK)的一个亚群,据报道其参与多种生物学过程,如基因表达、DNA损伤以及细胞激活/增殖/死亡途径。越来越多的研究表明,JNK信号通路的异常调节与组织纤维化密切相关。

综述目的

本综述旨在总结JNK信号通路在器官纤维化中作用的分子机制进展,希望为解决组织纤维化提供新的治疗策略。

综述的关键科学概念

最近的证据表明,JNK信号通路可调节器官纤维化中的炎症、免疫反应、氧化应激及多种细胞生物学功能。因此,靶向JNK通路可能是治疗纤维化的有效策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ed6/12302471/36bbfb404263/gr7.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ed6/12302471/82329a34bc51/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ed6/12302471/0f682055a748/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ed6/12302471/4699488bdb46/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ed6/12302471/8aa73f741e7f/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ed6/12302471/0e973461bdc6/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ed6/12302471/36bbfb404263/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ed6/12302471/0c7a98bbe1b1/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ed6/12302471/70b03b40a295/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ed6/12302471/82329a34bc51/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ed6/12302471/0f682055a748/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ed6/12302471/4699488bdb46/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ed6/12302471/8aa73f741e7f/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ed6/12302471/0e973461bdc6/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2ed6/12302471/36bbfb404263/gr7.jpg

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