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Emerging therapy strategies for energy metabolism in acute myocardial infarction
Ruixin Ma1,2,3,4,5, Dazhou Lu1,2,3,4,5, Zeyu Yang1,2,3,4,5
1Department of Emergency Medicine, Qilu Hospital of Shandong University, Jinan, 250012, China.
Insights
Acute myocardial infarction (AMI) triggers heart cell injury via disrupted energy metabolism. Targeting metabolic reprogramming and mitochondrial function shows promise for treating ischaemia-reperfusion injury (IRI) and improving outcomes.
Area of Science:
- Cardiovascular Medicine
- Cellular Metabolism
- Biochemistry
Background:
- Acute myocardial infarction (AMI) causes irreversible cardiomyocyte injury due to ischaemia and hypoxia.
- Ischaemia-reperfusion injury (IRI) exacerbates complications like arrhythmias and heart failure post-AMI.
- Myocardial energy metabolism is critically disrupted during AMI and IRI.
Purpose of the Study:
- To review the role of myocardial energy metabolism in AMI pathogenesis.
- To explore mechanisms of cellular injury during ischaemia-reperfusion.
- To discuss emerging therapeutic strategies for mitigating IRI.
Main Methods:
- Literature review integrating preclinical and clinical evidence.
- Focus on dysregulation of fatty acid oxidation, glycolysis, and mitochondrial function.
- Analysis of key injury mechanisms: ROS overproduction, succinate accumulation, mPTP opening.
Main Results:
- AMI disrupts myocardial energy metabolism, impacting FAO, glycolysis, and mitochondrial function.
- ROS, succinate accumulation, and mPTP opening are key drivers of IRI.
- Metabolic reprogramming, mitochondrial protection, and ischaemic conditioning are promising therapeutic avenues.
Conclusions:
- Metabolic modulation is a significant approach to mitigate IRI in AMI.
- Targeting cellular energy pathways offers potential for improved patient outcomes.
- Further research into metabolic interventions is warranted for AMI treatment.
Abstract:
Acute myocardial infarction (AMI) is a life-threatening cardiovascular event caused by the sudden blockage of a coronary artery, usually triggered by thrombotic events. This leads to significant myocardial ischaemia and hypoxia, disrupting the heart's energy metabolism and ultimately resulting in irreversible injury to cardiomyocytes. Despite advancements in reperfusion therapies, ischaemia-reperfusion injury (IRI) remains a critical contributor to complications such as arrhythmias and heart failure. This review explores the pivotal role of myocardial energy metabolism in AMI pathogenesis, focusing on the dysregulation of fatty acid oxidation (FAO), glycolysis, and mitochondrial dysfunction during ischaemia-reperfusion. Key mechanisms, including the overproduction of reactive oxygen species (ROS), succinate accumulation, and the opening of the mitochondrial permeability transition pore (mPTP), are highlighted as drivers of cellular injury. Emerging therapeutic strategies targeting metabolic reprogramming, mitochondrial protection, and ischaemic conditioning are discussed, highlighting their potential to mitigate IRI. By integrating preclinical and clinical evidence, this review highlights the promise of metabolic modulation as a significant approach to enhancing outcomes in AMI patients.
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