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.

中文翻译：

---

JNK 信号通路在器官纤维化中的作用

 背景

纤维化是由多种致病因素引起的组织损伤修复反应，几乎每个器官都可能发生，导致组织结构损伤、生理异常，甚至器官衰竭直至死亡。到目前为止，仍然没有特定的药物或策略可以有效阻断或改变组织纤维化。JNK 是丝裂原活化蛋白激酶 （MAPK） 的一个子集，据报道参与各种生物过程，例如基因表达、DNA 损伤和细胞活化/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

本文旨在总结 JNK 信号通路在器官纤维化中作用的分子机制进展，以期为解决组织纤维化提供一种新的治疗策略。

综述的关键科学概念

最近的证据表明，JNK 信号通路可以调节器官纤维化中的炎症、免疫反应、氧化应激和多种细胞生物学功能。因此，靶向 JNK 通路可能是治愈纤维化的有用策略。