ArticleCardiovascular drugs and therapy2025
Kirenol Ameliorates Myocardial Ischemia-Reperfusion Injury by Promoting Mitochondrial Function and Inhibiting Inflammasome Activation.
Article in Cardiovascular drugs and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Cardioprotection with Intralipid during CABG.Cardiovascular drugs and therapy · 2026Article
- MicroRNAs and Long Non-coding RNAs Associated With Sirtuin Pathways in Myocardial Ischemia/Reperfusion Injury.Cardiovascular drugs and therapy · 2026Review
- Cell death in ischemia-reperfusion injury: beyond a single-cell-death perspective.Biomarker research · 2026Review
- Dying for Clarity: Common Pitfalls in Cardiac Cell Death Research.Cardiovascular drugs and therapy · 2026Article
- Mitochondria at the Heart of Ischemia-Reperfusion (I/R) Injury: the HOXB5-Sirt5 Axis.Cardiovascular drugs and therapy · 2026Article
- Macrophage Polarization in Myocardial Ischemia‒Reperfusion Injury: Pathophysiology and Therapeutic Targets.Drug design, development and therapy · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
purposeMacrophage-mediated inflammation plays a crucial role in the pathophysiological process of myocardial ischemia/reperfusion (I/R) injury. Recent studies have highlighted the importance of mitochondrial function and inflammasome activation in the inflammatory process. Kirenol, a well-known natural compound, has been shown to regulate inflammation in various diseases. This study investigated whether Kirenol could exert anti-inflammatory effects on macrophages during myocardial I/R injury.
methodsMouse myocardial I/R models were established by 45 min of ischemia followed by 24 h of reperfusion. Saline or Kirenol treatment was administered. In vivo assessments included the evaluation of cardiac function, infarcted area, and immune cell infiltration. Subsequently, bone marrow-derived macrophages (BMDMs) were isolated, and mitochondrial function and pyroptosis were assessed. Furthermore, the study compared the cardioprotective effects of Kirenol with a specific NOX1/NOX4 inhibitor, GKT137831.
resultsKirenol gavage improved cardiac function, decreased infarct area, and alleviated inflammatory infiltration in mice subjected to myocardial I/R injury. Mechanistically, Kirenol inhibited NOX1 and NOX4 and enhanced mitochondrial function, ultimately attenuating the pyroptosis of macrophages. The therapeutic effects of Kirenol and GKT137831 were not significantly different.
conclusionThis study demonstrates that Kirenol mitigates myocardial I/R injury by inhibiting NOX1 and NOX4, restoring mitochondrial function, and ameliorating macrophage pyroptosis.
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Registered trials
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