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Updated: Jan 25, 2026

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
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MiR-153 regulates cardiomyocyte apoptosis by targeting Nrf2/HO-1 signaling

Xianting Zhu1, Yuling Zhao2, Wei Hou2

  • 1Department of Nursing, Yidu Central Hospital of Wei Fang, No. 4138, South Linglongshan Road, Weifang, 262500, Shandong, China.

Chromosome Research : an International Journal on the Molecular, Supramolecular and Evolutionary Aspects of Chromosome Biology
|May 1, 2019
PubMed

Insights

MicroRNA-153 (miR-153) promotes heart cell death after ischemia/reperfusion injury by increasing oxidative stress. Inhibiting miR-153 or boosting Nrf2 may prevent heart damage.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Cell Biology

Background:

  • MicroRNAs (miRNAs) are key regulators in human diseases, including cardiovascular conditions.
  • MiR-153 is known to influence neuron survival in cerebral ischemia/reperfusion (I/R) injury.
  • The role of miR-153 in I/R-induced cardiomyocyte apoptosis is not well understood.

Purpose of the Study:

  • To investigate the function of miR-153 in I/R-induced cardiomyocyte apoptosis.
  • To identify the molecular signaling pathway through which miR-153 affects cardiomyocytes during I/R injury.

Main Methods:

  • Utilized an oxygen-glucose deprivation and reoxygenation (OGD/R) cellular model to mimic I/R conditions in cardiomyocytes.
  • Assessed miR-153 levels, reactive oxygen species (ROS) production, and apoptosis signaling.
  • Identified downstream targets of miR-153, focusing on the Nrf2/HO-1 pathway.

Main Results:

  • OGD/R treatment significantly upregulated miR-153 in cardiomyocytes, leading to increased ROS and apoptosis.
  • Suppression of miR-153 demonstrated a protective effect against OGD/R-induced cardiomyocyte injury.
  • Nuclear factor-like 2 (Nrf2) was identified as a direct functional target of miR-153.
  • The Nrf2/heme oxygenase-1 (HO-1) signaling pathway was found to be crucial in miR-153-mediated apoptosis.

Conclusions:

  • miR-153 promotes cardiomyocyte apoptosis during I/R injury via ROS production and activation of apoptotic signaling.
  • The Nrf2/HO-1 pathway is a key mediator of miR-153's effects on cardiomyocytes.
  • Inhibiting miR-153 or restoring Nrf2 function presents a potential therapeutic avenue for preventing I/R injury.
Keywords:
ApoptosisCardiomyocytesIschemia/reperfusionNrf2miR-153

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