AI Article Synopsis
- Myocardial ischemia/reperfusion (I/R) injury happens when blood flow returns to the heart after a heart attack, causing damage.
- A study looked at a special protein called IF1 that helps protect heart cells from being harmed during this process by keeping energy levels stable.
- Researchers found that boosting IF1 in heart cells can help them recover and work better after injury, suggesting it could be a good target for treating heart problems.
Article Abstract
Myocardial ischemia/reperfusion (I/R) injury is a common clinic scenario that occurs in the context of reperfusion therapy for acute myocardial infarction (AMI). The mitochondrial F1Fo-ATPase inhibitory factor 1 (IF1) blocks the reversal of the F1Fo-ATP synthase to prevent detrimental consumption of cellular ATP and associated demise. In the present study, we study the role and mechanism of IF1 in myocardial I/R injury. Mice were ligated the left anterior descending coronary artery to build the I/R model . Rat hearts were isolated and perfused with constant pressure according to Langendorff. Also, neonatal cardiomyocytes hypoxia-reoxygenation (H/R) model was also used. Myocardial infarction area, cardiac function, cellular function, and cell viability was conducted and compared. Our data revealed that IF1 is upregulated in hearts after I/R and cardiomyocytes with hypoxia/re-oxygenation (H/R). IF1 delivered with adenovirus and adeno-associated virus serotype 9 (AAV9) ameliorated cardiac dysfunction and pathological development induced by I/R and . Mechanistically, IF1 stimulates glucose uptake and glycolysis activity and stimulates AMPK activation during basal and I/R and OGD/R conditions, and activation of AMPK by IF1 is responsible for its cardioprotective effects against H/R-induced injury. These results suggest that increased IF1 in the I/R heart confer cardioprotective effects via activating AMPK signaling. Therefore, IF1 can be used as a potential therapeutic target for the treatment of pathological ischemic injury and heart failure.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8741848 | PMC |
| http://dx.doi.org/10.7150/ijbs.64956 | DOI Listing |
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