Related Experiment Video
Updated: Jun 11, 2025

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
Published on: August 23, 2024
The role of JNK signaling pathway in organ fibrosis
Zhouhui Yao1, Yandan Lu2, Pingping Wang2
1School 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.
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.
Insights
Fibrosis, a damaging tissue repair response, lacks effective treatments. This review explores how the JNK signaling pathway contributes to organ fibrosis, suggesting it as a potential therapeutic target.
Area of Science:
- Molecular Biology
- Cellular Biology
- Pathology
Background:
- Fibrosis is a detrimental tissue repair response to injury, leading to organ damage and failure.
- Current treatments for fibrosis are limited, highlighting the need for novel therapeutic strategies.
- The c-Jun N-terminal kinase (JNK) signaling pathway is implicated in various cellular processes and is increasingly linked to fibrotic diseases.
Purpose of the Study:
- To review the molecular mechanisms of JNK signaling in organ fibrosis.
- To explore the potential of targeting the JNK pathway for novel anti-fibrotic therapies.
Main Methods:
- Literature review of studies investigating JNK signaling in fibrosis.
- Analysis of molecular pathways modulated by JNK in fibrotic conditions.
Main Results:
- JNK signaling pathway regulates inflammation, immune responses, and oxidative stress in fibrosis.
- Abnormal JNK pathway regulation is strongly associated with the development and progression of organ fibrosis.
- JNK pathway modulates multiple cellular functions critical to fibrotic processes.
Conclusions:
- Targeting the JNK signaling pathway presents a promising therapeutic strategy for treating organ fibrosis.
- Understanding JNK's role in fibrosis could lead to the development of effective anti-fibrotic drugs.
- Further research into JNK pathway modulation may offer new hope for patients suffering from fibrotic diseases.
More Related Videos
09:16Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
Published on: June 3, 2018
08:55Fabrication and Characterization of Layer-By-Layer Janus Base Nano-Matrix to Promote Cartilage Regeneration
Published on: July 6, 2022
Related Concept Videos
The JAK-STAT Signaling Pathway
MAPK Signaling Cascades
NF-κB-dependent Signaling Pathway
NF-κB-dependent Signaling Mechanism
The...
TGF - β Signaling Pathway
Interactions Between Signaling Pathways
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
PI3K/mTOR/AKT Signaling Pathway