Metabolic Remodeling in Failing Hearts
The healthy heart relies predominantly on fatty acid oxidation for energy, but in heart failure, metabolic remodeling shifts substrate utilization toward glucose and ketone metabolism. While this adaptation may initially preserve ATP production, over time, metabolic inflexibility worsens contractile dysfunction, oxidative stress, and mitochondrial inefficiency. Disruptions in nutrient signaling pathways, including AMPK and mTOR, further exacerbate the energy deficit characteristic of failing myocardium.
Targeting metabolic remodeling offers a novel therapeutic window. SGLT2 inhibitors have redefined heart failure management not only through diuresis but also by favorably altering myocardial energetics and promoting ketone utilization. Other approaches under study include metabolic modulators like trimetazidine, agents enhancing mitochondrial biogenesis, and gene therapies targeting defective oxidative pathways. This track will present insights into metabolic shifts in heart failure, highlight breakthroughs in metabolic-targeted drugs, and discuss how precision strategies may restore energetic balance and improve functional capacity in patients.
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