AI Article Synopsis
- Myocardial arrhythmia is a serious complication of ischemia-reperfusion injury in diabetic patients, and the study investigates the protective role of irisin against this issue.
- In an experiment with diabetic rats, irisin treatment showed a significant reduction in both the severity and occurrence of arrhythmias following I/R injury, affecting key proteins related to mitochondrial health, ER stress, and pyroptosis.
- The results indicate that irisin may provide a therapeutic approach for managing arrhythmias in diabetic patients by improving mitochondrial function while reducing ER stress and pyroptosis, although further research is needed to validate its effectiveness in humans.
Article Abstract
Objectives: Myocardial arrhythmia is a major complication of ischemia-reperfusion (I/R) injury in patients with diabetes. Irisin has significant cardioprotective effects, while its role in the pathophysiology of I/R injury-induced myocardial arrhythmia in the presence of diabetes is not well identified. Here, we aimed to investigate the potential antiarrhythmic impacts and mechanisms (mitochondrial biogenesis, endoplasmic reticulum (ER) stress, and pyroptosis) by which irisin reduces I/R injury-induced myocardial arrhythmia in diabetic rats.
Materials And Methods: Thirty high-fat diet-induced diabetic rats were subjected to I/R injury and myocardial arrhythmia. Irisin (0.5 μg/kg/day) was injected intraperitoneally before induction of I/R injury. Electrocardiography was used to measure the incidence and severity of ventricular arrhythmias. ELISA and western blotting analyses were employed to quantify the expression of mitochondrial biogenesis, ER stress, and pyroptosis-related proteins in ischemic myocardium.
Results: Irisin treatment in diabetic rats significantly decreased the lactate dehydrogenase level and the number and severity of arrhythmia induced by I/R injury. Irisin up-regulated the expression of mitochondrial biogenesis-related proteins while down-regulating the expression of ER stress and pyroptosis-related proteins. Furthermore, the inhibition of mitochondrial quality control by mdivi-1 significantly abolished the cardioprotective effect of irisin.
Conclusion: Our findings suggest that irisin reduced myocardial arrhythmia induced by I/R injury in diabetic rats by modulating the interaction of mitochondrial biogenesis and ER stress proteins and inhibiting the pyroptosis pathway. These findings provide a promising strategy for managing myocardial arrhythmia in diabetic patients, but supplementary studies are needed to confirm the clinical efficacy of irisin in these patients.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11459340 | PMC |
| http://dx.doi.org/10.22038/ijbms.2024.78069.16878 | DOI Listing |
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