Metabolic Modulation in Cardiovascular Health
Summary
Metabolic modulation refers to the deliberate adjustment of cellular energy pathways to enhance cardiovascular performance and resilience. In healthy hearts, metabolic flexibility allows efficient switching between fatty acids, glucose and ancillary substrates such as lactate or ketone bodies in response to changing workload and oxygen availability. In pathological states – including ischaemic heart disease, diabetic cardiomyopathy and heart failure – this flexibility is diminished, resulting in energy deficits, accumulation of toxic intermediates and maladaptive remodelling. Recent advances have elucidated key molecular regulators of substrate selection, notably AMP-activated protein kinase (AMPK), peroxisome proliferator-activated receptor α (PPARα) and the SIRT1 axis, which coordinate shifts towards oxygen-sparing glucose oxidation and enhanced mitochondrial biogenesis. Therapeutic agents that fine-tune these pathways, such as trimetazidine and emerging small-molecule AMPK activators, have shown promise in restoring energetics, reducing oxidative stress and improving contractile function. Beyond the myocardium, metabolic interventions also ameliorate endothelial dysfunction by normalising nitric oxide availability and attenuating inflammation. Together, these findings underscore the global significance of targeting metabolic networks to prevent disease progression, improve clinical outcomes and pave the way for personalised cardiovascular medicine.
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Metabolic Modulation in Cardiovascular Health publication trend
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Technical terms
Metabolic modulation: Strategic alteration of cellular energy substrate use to optimise efficiency and function.
Endothelial dysfunction: Impairment of the vascular endothelium’s capacity to regulate vascular tone and maintain homeostasis.
Adenosine monophosphate-activated protein kinase (AMPK): A central cellular energy sensor that promotes energy-generating pathways under stress.
Peroxisome proliferator-activated receptor α (PPARα): Nuclear receptor that regulates genes involved in fatty acid uptake and oxidation.
Ketone body metabolism: Catabolism and utilisation of ketone bodies as alternative cardiac energy substrates during metabolic stress.
References
- Role of Trimetazidine in Ameliorating Endothelial Dysfunction: A Review. Pharmaceuticals (2024).
- Trimetazidine in Heart Failure. Frontiers in Pharmacology (2021).
- Trimetazidine Ameliorates Myocardial Metabolic Remodeling in Isoproterenol-Induced Rats Through Regulating Ketone Body Metabolism via Activating AMPK and PPAR α. Frontiers in Pharmacology (2020).
- Function and Mechanism of Trimetazidine in Myocardial Infarction-Induced Myocardial Energy Metabolism Disorder Through the SIRT1–AMPK Pathway. Frontiers in Physiology (2021).
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