Epigenetic control of inflammation

We investigate how chromatin-regulating enzymes shape immune activation in health and disease. Building on earlier work dissecting epigenetic regulation of myeloid differentiation and leukemogenesis in acute myeloid leukemia, we now apply similar mechanistic frameworks to chronic inflammatory settings.

Using CRISPR-based perturbation screens combined with transcriptomic profiling, we map how histone-modifying enzymes—including KDM5C, KAT2B, PRMT6, and CARM1—influence macrophage and monocyte responses to inflammatory stimuli. These enzymes act through distinct chromatin mechanisms such as histone demethylation, acetylation, and arginine methylation, converging on transcriptional networks that fine-tune inflammatory tone.

Follow-up studies in knockout models and patient-derived macrophages integrate transcriptomic, epigenomic, and functional assays to dissect how these regulators maintain immune homeostasis or drive chronic inflammation. By linking chromatin remodeling to immune activation, we aim to define actionable mechanisms underlying inflammation in cardiometabolic disease.

Immune–stromal crosstalk in cardiometabolic disease

We study how immune cells interact with metabolic and vascular tissues to sustain chronic inflammation. Through large-scale single-cell and spatial transcriptomic profiling of human patient cohorts and tissue biobanks, we reconstruct immune–stromal communication networks driving metabolic dysfunction in cardiometabolic diseases such as obesity, MASLD, and atherosclerosis.

As part of these efforts, we contributed to one of the first single-cell atlases of human atherosclerotic plaques, which revealed distinct macrophage and stromal phenotypes linked to plaque stability and inflammation. These efforts build on close integration with translational cohorts, including longitudinal and intervention studies, to connect molecular changes to clinical outcomes.

In the long term, we aim to translate these insights into predictive models that may help refine patient selection for metabolic surgery and guide more personalized treatment strategies in cardiometabolic disease.