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MST1-Hippo pathway regulates inflammation response following myocardial infarction through inhibiting HO-1 signaling

Yanan Tian1, Haijiu Song2, Dapeng Jin1

  • 1Department of Cardiology, The Affiliated Hospital of Chengde Medical College, Chengde, P. R. China.

Journal of Receptor and Signal Transduction Research
|February 15, 2020
PubMed

Insights

Mammalian STE20-like protein kinase 1 (MST1) exacerbates inflammation and cardiomyocyte damage after myocardial infarction. Inhibiting MST1 protects heart cells by boosting heme oxygenase-1 (HO-1) signaling.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Biochemistry

Background:

  • Mammalian STE20-like protein kinases 1 (MST1) is linked to cardiomyocyte damage post-myocardial infarction (MI).
  • Understanding MST1's role in the inflammatory response following MI is crucial for developing new therapies.

Purpose of the Study:

  • To investigate the specific influence of MST1 on the inflammation response in cardiomyocytes after myocardial infarction.
  • To elucidate the molecular mechanisms by which MST1 affects cardiomyocyte survival and inflammation.

Main Methods:

  • Established an in vitro myocardial infarction model using a cardiomyocyte cell line exposed to hypoxia.
  • Utilized ELISA, qPCR, Western blots, and siRNA technology to analyze MST1's role and expression.
  • Assessed the impact of MST1 deletion on heme oxygenase-1 (HO-1) activity and cardiomyocyte death.

Main Results:

  • MST1 transcription and expression were significantly elevated in the myocardial infarction model.
  • Loss of MST1 attenuated inflammatory responses and improved cardiomyocyte survival in vitro.
  • MST1 deletion reversed heme oxygenase-1 (HO-1) activity, reducing hypoxia-mediated cardiomyocyte death.

Conclusions:

  • The MST1-Hippo pathway is activated during myocardial infarction, contributing to inflammation.
  • MST1 inhibition promotes cardiomyocyte survival by upregulating the HO-1 signaling pathway.
  • Targeting the MST1-Hippo-HO-1 axis offers a potential therapeutic strategy for myocardial infarction.

Keywords:
HO-1MST1cardiomyocyteinflammation responsemyocardial infarction

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