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NURR1 inhibition reduces hypoxia-mediated cardiomyocyte necrosis via blocking Mst1-JNK-mPTP pathway

Guanqun Ma1, Yingwu Liu1

  • 1Department of Cardiology, The Third Central Hospital of Tianjin, Tianjin, China.

Journal of Receptor and Signal Transduction Research
|November 23, 2019
PubMed

Insights

Nuclear receptor related 1 protein (NURR1) promotes cardiomyocyte death under hypoxia by activating the Mst1-JNK-mPTP pathway. Deleting NURR1 enhances cardiomyocyte survival and reduces necrosis.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Cell Death Mechanisms

Background:

  • Hypoxia significantly damages cardiomyocytes, but the role of necrosis in this process requires further investigation.
  • Nuclear receptor related 1 protein (NURR1) is implicated in cellular stress responses.

Purpose of the Study:

  • To investigate the pathological role of NURR1 in regulating cardiomyocyte viability under hypoxia.
  • To elucidate the molecular mechanisms by which NURR1 influences cardiomyocyte death.

Main Methods:

  • Cardiomyocytes were subjected to hypoxia and treated with siRNA against NURR1.
  • The Mst1-JNK-mPTP pathway was modulated using pathway agonists.
  • Cell viability, death, and inflammatory responses were assessed.

Main Results:

  • NURR1 expression increased under hypoxia, and NURR1 knockout promoted cardiomyocyte survival and reduced necrosis.
  • NURR1 upregulation activated the Mst1-JNK pathway, leading to mitochondrial permeability transition pore (mPTP) opening and cardiomyocyte necrosis.
  • Re-activating the Mst1-JNK pathway abolished the protective effects of NURR1 deletion.

Conclusions:

  • Hypoxia-induced cardiomyocyte death involves NURR1 upregulation.
  • NURR1 contributes to cardiomyocyte necrosis by activating the Mst1-JNK-mPTP pathway.
  • Targeting NURR1 may offer a therapeutic strategy for hypoxia-related heart damage.
Keywords:
Mst1NURR1cardiomyocyteshypoxianecrosis

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