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The Protective Role of ILC3s Glycolysis in Myocardial Ischemia-Reperfusion Injury: Unveiling Metabolic and Immune Regulatory Mechanisms

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Myocardial ischemia-reperfusion injury (MIRI) is a pathological process where the myocardium suffers further damage after blood flow is restored, posing a significant threat to patient health. Traditional treatment methods have many limitations, while innate lymphoid cells type 3 (ILC3s) and their glycolysis have shown important functions and great potential in MIRI. ILC3s, originating from common lymphoid progenitors, are widely distributed in various tissues and possess multiple functions such as anti-inflammation, immune balance regulation, promotion of cardiomyocyte regeneration, enhancement of cell survival, and activation of endogenous protective mechanisms, all of which rely on their glycolysis process. ILC3s glycolysis affects the pathological and physiological process of MIRI and its prognosis through mechanisms involving glucose uptake, metabolic pathways, metabolic sensing molecules, signal transduction pathways, cytokine secretion, metabolic product signaling, antioxidant enzyme and reactive oxygen species regulation, and apoptosis signaling pathways. In terms of treatment, key enzymes, metabolic sensing molecules, and signaling pathways in the glycolysis pathway of ILC3s are expected to become new therapeutic targets. Activating ILC3s glycolysis can promote cardiomyocyte regeneration and repair, enhance cell survival, and improve clinical prognosis. Moreover, the regulation of ILC3s glycolysis can be combined with drug therapy, ischemic preconditioning, stem cell therapy, and other means to exert synergistic effects. By detecting the glycolysis characteristics and ILC3s functional status of patients, it is hoped to achieve precision and individualization in MIRI treatment. However, current research still faces many challenges, including incomplete understanding of the specific mechanisms of ILC3s glycolysis, insufficient precision and effectiveness of regulatory means, and clinical transformation limited by patient individual differences and ethical considerations. In the future, it is necessary to strengthen the combination of basic research and clinical application, break through these barriers, fully explore the application value of ILC3s glycolysis in MIRI treatment, provide more effective treatment plans for patients, and improve survival quality and prognosis.
Title: The Protective Role of ILC3s Glycolysis in Myocardial Ischemia-Reperfusion Injury: Unveiling Metabolic and Immune Regulatory Mechanisms
Description:
Myocardial ischemia-reperfusion injury (MIRI) is a pathological process where the myocardium suffers further damage after blood flow is restored, posing a significant threat to patient health.
Traditional treatment methods have many limitations, while innate lymphoid cells type 3 (ILC3s) and their glycolysis have shown important functions and great potential in MIRI.
ILC3s, originating from common lymphoid progenitors, are widely distributed in various tissues and possess multiple functions such as anti-inflammation, immune balance regulation, promotion of cardiomyocyte regeneration, enhancement of cell survival, and activation of endogenous protective mechanisms, all of which rely on their glycolysis process.
ILC3s glycolysis affects the pathological and physiological process of MIRI and its prognosis through mechanisms involving glucose uptake, metabolic pathways, metabolic sensing molecules, signal transduction pathways, cytokine secretion, metabolic product signaling, antioxidant enzyme and reactive oxygen species regulation, and apoptosis signaling pathways.
In terms of treatment, key enzymes, metabolic sensing molecules, and signaling pathways in the glycolysis pathway of ILC3s are expected to become new therapeutic targets.
Activating ILC3s glycolysis can promote cardiomyocyte regeneration and repair, enhance cell survival, and improve clinical prognosis.
Moreover, the regulation of ILC3s glycolysis can be combined with drug therapy, ischemic preconditioning, stem cell therapy, and other means to exert synergistic effects.
By detecting the glycolysis characteristics and ILC3s functional status of patients, it is hoped to achieve precision and individualization in MIRI treatment.
However, current research still faces many challenges, including incomplete understanding of the specific mechanisms of ILC3s glycolysis, insufficient precision and effectiveness of regulatory means, and clinical transformation limited by patient individual differences and ethical considerations.
In the future, it is necessary to strengthen the combination of basic research and clinical application, break through these barriers, fully explore the application value of ILC3s glycolysis in MIRI treatment, provide more effective treatment plans for patients, and improve survival quality and prognosis.

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