ArticleAmerican journal of translational research2025
Hemin-induced HO-1 protects isolated rat hearts from ischemia-reperfusion injury by activation of pro-survival signalling pathways.
Article in American journal of translational research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Abstract
objectivesMyocardial ischemia-reperfusion (I/R) injury significantly contributes to cardiac dysfunction and increased mortality following myocardial infarction (MI). Heme oxygenase-1 (HO-1), a stress-inducible enzyme playing a key role in degrading heme into biliverdin, carbon monoxide (CO), and free iron, all of which possess cytoprotective properties. This study aimed to investigate the effects of pharmacological modulation of HO-1 on myocardial I/R injury in isolated rat hearts and to elucidate the underlying mechanisms of HO-1-mediated cardioprotection.
methodsUsing a Langendorff perfusion system, rat hearts were subjected to controlled I/R in the presence and absence of HO-1 modulators such as Hemin and Zinc Protoporphyrin IX. To check the possible involvement of various cardioprotective signalling pathways, their inhibitors were used. Hemodynamic and cardiodynamic data, cardiac injury markers, oxidative stress markers, and histopathologic changes were evaluated.
resultsOur results reveal that HO-1 induction by Hemin confers substantial protection against I/R injury by preserving cardiac function, and reducing myocardial injury and oxidative stress. However, this cardioprotective effect of HO-1 was either partially or completely abolished upon inhibition of specific pro-survival pathways, including phosphoinositide 3-kinase (PI3K), protein kinase C (PKC), nitric oxide synthase (NOS), and ATP-sensitive potassium (K
conclusionHO-1 induction by Hemin protects the myocardium against I/R injury through activation of multiple pro-survival signalling pathways, supporting its potential as a therapeutic target for myocardial infarction.
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