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Updated: Oct 18, 2025

Visualization of Cell Cycle Variations and Determination of Nucleation in Postnatal Cardiomyocytes
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The circRNA CNEACR regulates necroptosis of cardiomyocytes through Foxa2 suppression

Xiang-Qian Gao1,2, Cui-Yun Liu1, Yu-Hui Zhang3

  • 1Institute for Translational Medicine, The Affiliated Hospital of Qingdao University, College of Medicine, Qingdao University, 266021, Qingdao, China.

Cell Death and Differentiation
|September 30, 2021
PubMed

Insights

Circular RNAs (circRNAs) protect heart cells from death after ischemia-reperfusion injury. This cardiac- necroptosis-associated circRNA (CNEACR) targets the HDAC7/Foxa2/RIPK3 pathway, improving cardiac function and reducing heart damage.

Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Cell Death Mechanisms

Background:

  • Circular RNAs (circRNAs) show altered expression in cardiovascular diseases like ischemia-reperfusion (I/R) injury.
  • The role of circRNAs in cardiomyocyte cell death, particularly necrotic forms, is not well understood.

Purpose of the Study:

  • To investigate the function of mmu_circ_000338 (CNEACR) in cardiomyocyte death during hypoxia-reoxygenation (H/R) and I/R injury.
  • To elucidate the molecular mechanism by which CNEACR influences necrotic cell death pathways.

Main Methods:

  • Assessed CNEACR levels in H/R-exposed cardiomyocytes and I/R-injured mouse hearts.
  • Enforced CNEACR expression to evaluate its effects on cardiomyocyte death and myocardial infarction.
  • Investigated the interaction of CNEACR with HDAC7 and its impact on Foxa2 transcription and RIPK3 regulation.

Main Results:

  • CNEACR levels were decreased in H/R cardiomyocytes and I/R hearts.
  • Enforced CNEACR expression reduced H/R-induced cardiomyocyte death and myocardial necrosis in I/R mice.
  • CNEACR attenuated myocardial infarction size and improved cardiac function.
  • Mechanistically, CNEACR inhibited HDAC7 nuclear entry, leading to increased Foxa2 transcription and subsequent suppression of RIPK3-dependent cell death.

Conclusions:

  • CNEACR plays a protective role against necrotic cell death in cardiomyocytes during I/R injury.
  • The CNEACR/HDAC7/Foxa2/RIPK3 axis represents a novel therapeutic target for mitigating myocardial damage in ischemic heart diseases.

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