Nicorandil in Myocardial Ischemia-Reperfusion Injury: Mechanisms of Cardioprotection

Corresponding author: GE Zhenrong, 1902141742@qq.com

DOI: 10.12201/bmr.202509.00032

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  Abstract: Myocardial ischemia-reperfusion injury (MIRI)following acute myocardial infarction (AMI) is a pivotal contributor to poor clinical prognosis.Nicorandil, a multifunctional agent combining nitrate-like effects and ATP-sensitive potassium (KATP) channel-opening activity, has recently achieved notable progress in mechanistic research for MIRI prevention and treatment. This review systematically elaborates the molecular basis of Nicorandil in attenuating myocardial injury through activation of mitochondrial KATP channels, inhibition of calcium overload, regulation of the IL-33/ST2 signaling pathway, and suppression of theTLR4/NF-κB/NLRP3 inflammatory axis. Clinical evidence indicates that Nicorandil enhances coronary blood flow (as evidenced by improved TIMI flow grades) post-percutaneous coronary intervention (PCI) and reduces the incidence of major adverse cardiovascular events (MACE). For the first time, this review consolidates Nicorandil’s dual anti-apoptotic and anti-inflammatory roles, offering a theoretical framework and clinical insights to optimize cardiovascular disease therapeutics.

  Key words: Nicorandil; Myocardial ischemia-reperfusion injury; Myocardial protection; Potassium channel opener; Mitochondrial protection; Apoptosis; Inflammatory response

  Submit time: 12 September 2025

  Copyright: The copyright holder for this preprint is the author/funder, who has granted biomedRxiv a license to display the preprint in perpetuity.
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