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<p>Ferroptosis occurs after myocardial ischemia–reperfusion (I/R) injury. Long non-coding RNA (lncRNA) AK020546 possesses the effect of protecting the myocardium from I/R injury; however, the underlying mechanisms remain not fully understood. This study aimed to investigate the effect of AK020546 on ferroptosis in cardiomyocytes and underlying molecular mechanisms. Hypoxia/reoxygenation (H/R) was used to induce H9C2 injury, and an I/R rat model was generated. Ferroptosis was evaluated by detecting lipid reactive oxygen species, Fe<sup>2+</sup>, glutathione, and malondialdehyde levels. The N(6)-methyladenosine (m6A) methylation of Mst1 was assessed by RNA binding protein immunoprecipitation (RIP), methylated-RIP, luciferase reporter assay, and RNA stability assay. The results showed that AK020546 inhibited H/R-induced ferroptosis. It also decreased Mst1 expression through binding with METTL14. Moreover, METTL14 promoted m6A methylation of Mst1, thereby enhancing its stability. METTL14 and Mst1 were involved in AK020546-mediated ferroptosis. Besides, AK020546 alleviated myocardial damage in I/R rats. In conclusion, the AK020546/METTL14/m6A-Mst1 axis protects against myocardial I/R injury by suppressing cardiomyocyte ferroptosis, suggesting a promising target for myocardial I/R injury.</p>

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LncRNA AK020546 Alleviates Myocardial Ischemia–Reperfusion Injury via Suppressing METTL14/m6A/MST1 Axis-Mediated Ferroptosis

  • 期刊论文

  • 发表日期：

    2025年6月4日

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  • Meiqi Zhang,
  • Qilan Chen,
  • Jie Chen,
  • Yun Chen,
  • Wei Zhang,
  • Yakun Wang,
  • Limei Yu,
  • Zhenfei Yu

摘要

Ferroptosis occurs after myocardial ischemia–reperfusion (I/R) injury. Long non-coding RNA (lncRNA) AK020546 possesses the effect of protecting the myocardium from I/R injury; however, the underlying mechanisms remain not fully understood. This study aimed to investigate the effect of AK020546 on ferroptosis in cardiomyocytes and underlying molecular mechanisms. Hypoxia/reoxygenation (H/R) was used to induce H9C2 injury, and an I/R rat model was generated. Ferroptosis was evaluated by detecting lipid reactive oxygen species, Fe2+, glutathione, and malondialdehyde levels. The N(6)-methyladenosine (m6A) methylation of Mst1 was assessed by RNA binding protein immunoprecipitation (RIP), methylated-RIP, luciferase reporter assay, and RNA stability assay. The results showed that AK020546 inhibited H/R-induced ferroptosis. It also decreased Mst1 expression through binding with METTL14. Moreover, METTL14 promoted m6A methylation of Mst1, thereby enhancing its stability. METTL14 and Mst1 were involved in AK020546-mediated ferroptosis. Besides, AK020546 alleviated myocardial damage in I/R rats. In conclusion, the AK020546/METTL14/m6A-Mst1 axis protects against myocardial I/R injury by suppressing cardiomyocyte ferroptosis, suggesting a promising target for myocardial I/R injury.