Main Content

Research Summary

My research focuses on cardiovascular immunometabolism, with a particular emphasis on how macrophage-driven inflammation and metabolic reprogramming influence tissue injury and repair following myocardial infarction (MI) and systemic inflammatory conditions such as sepsis. Using integrated in vivo mouse models, ex vivo cellular systems, and multi-omics approaches (transcriptomics, metabolomics, and functional metabolic assays), I investigate how metabolic substrates such as lactate and ketone bodies regulate immune cell function and tissue remodeling.

My current work examines the role of ketone metabolism in modulating macrophage polarization, mitochondrial function, and inflammasome activation after MI. Specifically, I investigate how monocarboxylate transporter 1 (MCT1)-dependent ketone uptake regulates the transition from pro-inflammatory to reparative macrophage phenotypes, with the goal of identifying novel therapeutic strategies to improve cardiac outcomes.

In parallel, I study immunometabolic dysregulation in sepsis, focusing on how systemic inflammation reshapes macrophage metabolism and contributes to organ dysfunction, including septic cardiomyopathy. Additionally, my research explores the pathological role of glycolysis and lactate production in cardiac fibroblast activation and fibrosis. By targeting key metabolic enzymes such as lactate dehydrogenase A (LDHA), I aim to define metabolic interventions that limit adverse remodeling and progression to heart failure.

Overall, my work integrates molecular biology, physiology, and computational analysis to uncover mechanistic links between metabolism and immune regulation across cardiovascular and inflammatory diseases, with a long-term goal of developing translational strategies to improve patient outcomes.