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Related Experiment Video

Updated: May 5, 2026

Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
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NR1D2 Knockdown Alleviates Myocardial Infarction through Nrf2 Signaling Pathway Activation.

Ting Wang1, Helong Xiao2, Meijian Yang3

  • 1Department of Cardiology, Hebei Medical University Third Hospital, No. 139, Ziqiang Road, Shijiazhuang, Hebei, China.

Cardiovascular Drugs and Therapy
|May 4, 2026
PubMed
Summary

Nuclear receptor subfamily 1 group D member 2 (NR1D2) worsens myocardial infarction (MI) by promoting ferroptosis. Targeting NR1D2 activates the protective nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, offering a novel therapeutic strategy for MI.

Keywords:
Inflammatory reactionMyocardial infarctionNuclear factor erythroid 2–related factor 2Nuclear receptor subfamily 1 group D member 2Signaling pathway

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Area of Science:

  • Cardiovascular Research
  • Cellular Biology
  • Molecular Medicine

Background:

  • Ferroptosis, a regulated form of cell death, plays a significant role in the pathogenesis of myocardial infarction (MI).
  • The specific role of nuclear receptor subfamily 1 group D member 2 (NR1D2) in MI-associated ferroptosis and its interaction with the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway remain largely unexplored.

Purpose of the Study:

  • To investigate whether NR1D2 regulates ferroptosis in myocardial infarction (MI) via the Nrf2 pathway.
  • To evaluate the potential therapeutic efficacy of NR1D2 knockdown in mitigating MI-induced ferroptosis and cardiac dysfunction.

Main Methods:

  • Bioinformatic analysis of Gene Expression Omnibus (GEO) datasets identified NR1D2 as a key ferroptosis-related gene in MI.
  • In vitro studies involved NR1D2 silencing in hypoxia/reoxygenation (H/R)-injured HL-1 cardiomyocytes, with Nrf2 pathway involvement confirmed using the inhibitor ML385.
  • A mouse model of MI was established to assess cardiac function following NR1D2 knockdown, with and without ML385 co-treatment.

Main Results:

  • NR1D2 expression was significantly upregulated in MI. Knockdown of NR1D2 in H/R-injured cardiomyocytes reduced cell death, inflammation, and ferroptosis markers (Fe²⁺, MDA, GSH/GSSG ratio).
  • These protective effects were abrogated by ML385, confirming Nrf2 pathway dependence. NR1D2 knockdown activated the Nrf2/HO-1 signaling axis, upregulating downstream effectors like GPX4 and SLC7A11.
  • In vivo, NR1D2 knockdown in MI mice improved cardiac function (EF, FS), reduced infarct size, and inhibited ferroptosis, effects negated by ML385.

Conclusions:

  • NR1D2 exacerbates MI injury by suppressing the Nrf2 pathway and promoting ferroptosis.
  • Targeting NR1D2 activates Nrf2 signaling, alleviating ferroptotic damage in MI.
  • NR1D2 represents a novel therapeutic target for myocardial infarction, offering a new strategy to combat ferroptosis-induced cardiac injury.