Gemfibrozil mitigates caspase-11-driven myocardial pyroptosis in ischemia/reperfusion injury in mice

The size of the infarct area following acute myocardial infarction (AMI) is a critical prognostic factor. Caspase-11-dependent pyroptosis has been implicated as a key mechanism driving cardiomyocyte death after AMI. However, no therapeutic agents have been developed to inhibit myocardial cell death...

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Main Authors: Tetsuro Marunouchi, Mayu Kyono, Naoko Kikuchi, Kouichi Tanonaka
Format: Article
Language:English
Published: Elsevier 2025-06-01
Series:Journal of Molecular and Cellular Cardiology Plus
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Online Access:http://www.sciencedirect.com/science/article/pii/S277297612500011X
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author Tetsuro Marunouchi
Mayu Kyono
Naoko Kikuchi
Kouichi Tanonaka
author_facet Tetsuro Marunouchi
Mayu Kyono
Naoko Kikuchi
Kouichi Tanonaka
author_sort Tetsuro Marunouchi
collection DOAJ
description The size of the infarct area following acute myocardial infarction (AMI) is a critical prognostic factor. Caspase-11-dependent pyroptosis has been implicated as a key mechanism driving cardiomyocyte death after AMI. However, no therapeutic agents have been developed to inhibit myocardial cell death by targeting caspase-11. This study investigates the effects of gemfibrozil, a potential caspase-11 inhibitor, on ischemia/reperfusion-induced myocardial pyroptosis in mice. To model AMI, the left coronary artery of C57BL/6 N mice was ligated for 1 h, followed by reperfusion. Levels of cleaved caspase-11 and the N-terminal fragment of gasdermin D (GSDMD-N) in ischemic myocardial tissue increased progressively over time after ischemia/reperfusion. Gemfibrozil treatment during reperfusion significantly attenuated these increases in cleaved caspase-11 and GSDMD-N levels. Moreover, gemfibrozil reduced the extent of myocardial infarct size during reperfusion. In cultured cardiomyocytes isolated from adult mice, hypoxia/reoxygenation-induced increases in caspase-11 and GSDMD cleavage were similarly mitigated by gemfibrozil, which concurrently prevented necrotic cell death. These findings demonstrate the involvement of caspase-11-dependent pyroptosis in myocardial cell death following ischemia/reperfusion and suggest that gemfibrozil holds promise as a therapeutic agent for reducing myocardial infarct size after AMI.
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publishDate 2025-06-01
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series Journal of Molecular and Cellular Cardiology Plus
spelling doaj-art-86dfbcfe52894c2b93c76f19724fbfdb2025-08-20T02:39:37ZengElsevierJournal of Molecular and Cellular Cardiology Plus2772-97612025-06-011210029210.1016/j.jmccpl.2025.100292Gemfibrozil mitigates caspase-11-driven myocardial pyroptosis in ischemia/reperfusion injury in miceTetsuro Marunouchi0Mayu Kyono1Naoko Kikuchi2Kouichi Tanonaka3Department of Molecular and Cellular Pharmacology, Tokyo University of Pharmacy and Life Sciences, JapanDepartment of Molecular and Cellular Pharmacology, Tokyo University of Pharmacy and Life Sciences, JapanDepartment of Molecular and Cellular Pharmacology, Tokyo University of Pharmacy and Life Sciences, JapanCorresponding author at: Department of Molecular and Cellular Pharmacology, Tokyo University of Pharmacy and Life Sciences, 1432-1 Horinouchi, Hachioji, Tokyo 192-0392, Japan.; Department of Molecular and Cellular Pharmacology, Tokyo University of Pharmacy and Life Sciences, JapanThe size of the infarct area following acute myocardial infarction (AMI) is a critical prognostic factor. Caspase-11-dependent pyroptosis has been implicated as a key mechanism driving cardiomyocyte death after AMI. However, no therapeutic agents have been developed to inhibit myocardial cell death by targeting caspase-11. This study investigates the effects of gemfibrozil, a potential caspase-11 inhibitor, on ischemia/reperfusion-induced myocardial pyroptosis in mice. To model AMI, the left coronary artery of C57BL/6 N mice was ligated for 1 h, followed by reperfusion. Levels of cleaved caspase-11 and the N-terminal fragment of gasdermin D (GSDMD-N) in ischemic myocardial tissue increased progressively over time after ischemia/reperfusion. Gemfibrozil treatment during reperfusion significantly attenuated these increases in cleaved caspase-11 and GSDMD-N levels. Moreover, gemfibrozil reduced the extent of myocardial infarct size during reperfusion. In cultured cardiomyocytes isolated from adult mice, hypoxia/reoxygenation-induced increases in caspase-11 and GSDMD cleavage were similarly mitigated by gemfibrozil, which concurrently prevented necrotic cell death. These findings demonstrate the involvement of caspase-11-dependent pyroptosis in myocardial cell death following ischemia/reperfusion and suggest that gemfibrozil holds promise as a therapeutic agent for reducing myocardial infarct size after AMI.http://www.sciencedirect.com/science/article/pii/S277297612500011XCaspase-11PyroptosisGemfibrozilIschemiaReperfusion
spellingShingle Tetsuro Marunouchi
Mayu Kyono
Naoko Kikuchi
Kouichi Tanonaka
Gemfibrozil mitigates caspase-11-driven myocardial pyroptosis in ischemia/reperfusion injury in mice
Journal of Molecular and Cellular Cardiology Plus
Caspase-11
Pyroptosis
Gemfibrozil
Ischemia
Reperfusion
title Gemfibrozil mitigates caspase-11-driven myocardial pyroptosis in ischemia/reperfusion injury in mice
title_full Gemfibrozil mitigates caspase-11-driven myocardial pyroptosis in ischemia/reperfusion injury in mice
title_fullStr Gemfibrozil mitigates caspase-11-driven myocardial pyroptosis in ischemia/reperfusion injury in mice
title_full_unstemmed Gemfibrozil mitigates caspase-11-driven myocardial pyroptosis in ischemia/reperfusion injury in mice
title_short Gemfibrozil mitigates caspase-11-driven myocardial pyroptosis in ischemia/reperfusion injury in mice
title_sort gemfibrozil mitigates caspase 11 driven myocardial pyroptosis in ischemia reperfusion injury in mice
topic Caspase-11
Pyroptosis
Gemfibrozil
Ischemia
Reperfusion
url http://www.sciencedirect.com/science/article/pii/S277297612500011X
work_keys_str_mv AT tetsuromarunouchi gemfibrozilmitigatescaspase11drivenmyocardialpyroptosisinischemiareperfusioninjuryinmice
AT mayukyono gemfibrozilmitigatescaspase11drivenmyocardialpyroptosisinischemiareperfusioninjuryinmice
AT naokokikuchi gemfibrozilmitigatescaspase11drivenmyocardialpyroptosisinischemiareperfusioninjuryinmice
AT kouichitanonaka gemfibrozilmitigatescaspase11drivenmyocardialpyroptosisinischemiareperfusioninjuryinmice