Mechanism and research progress of MAPK signaling pathway in myocardial fibrosis

Jinqiao Wu1, Min Chen1, Ze Peng1

  • 1First Clinical Medical College, Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang, China.

PubMed

Insights

Myocardial fibrosis, a key cardiac remodeling factor, involves p38 MAPK, JNK, and ERK pathways. This review explores their roles and therapeutic targets for cardiovascular disease.

Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Pathology

Background:

  • Myocardial fibrosis (MF) is a significant pathological outcome in various cardiovascular diseases.
  • MF is a critical component of cardiac remodeling processes.
  • Specific signaling pathways, including p38 MAPK, JNK, and ERK, are implicated in the development of MF.

Purpose of the Study:

  • To review the roles and intricate interactions of p38 MAPK, JNK, and ERK signaling pathways in myocardial fibrosis.
  • To identify and summarize current and emerging drug and non-pharmacological therapies targeting these pathways for MF treatment.

Main Methods:

  • Literature review of scientific publications.
  • Analysis of signaling pathway mechanisms in cardiac remodeling.
  • Synthesis of information on therapeutic interventions.

Main Results:

  • Detailed explanation of how p38 MAPK, JNK, and ERK pathways contribute to MF.
  • Identification of key molecular interactions within these pathways during fibrosis.
  • Overview of pharmacological agents and lifestyle interventions targeting these pathways.

Conclusions:

  • The p38 MAPK, JNK, and ERK pathways are crucial regulators of myocardial fibrosis.
  • Targeting these signaling pathways presents a promising therapeutic strategy for cardiovascular diseases characterized by MF.
  • Further research into combined and novel therapies is warranted.

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