Sona Kang

Research Bio

The central goal of the Kang Lab is to advance understanding of the epigenetic and molecular mechanisms shaping metabolic homeostasis, ultimately seeking innovative paths to treat obesity, type 2 diabetes, and related metabolic diseases. They employ a multidisciplinary approach, integrating cellular and animal models with advanced molecular, biochemical, and genomic tools to dissect the complex regulatory networks underpinning adipose tissue and skeletal muscle function, and how tissue-intrinsic programs coordinate systemic energy balance.

Adipose tissue is a crucial endocrine organ, secreting hormones and signaling molecules that regulate appetite, insulin sensitivity, inflammation, and energy expenditure throughout the body. Understanding how epigenetic and intracellular signaling pathways shape these endocrine functions in adipose tissue is central to our research.

In adipose tissue, they focus on defining how epigenetic enzymes and signaling pathways orchestrate metabolism, thermogenesis, and tissue development and plasticity. Their work has revealed an intricate epigenetic push-pull: DNMT3A promotes insulin resistance, whereas TET2 facilitates PPARγ-driven insulin sensitization. They are exploring how TET3 shapes adipocyte precursor cell development and diet-induced remodeling through regulation of extracellular matrix dynamics and PPARγ signaling. Additionally, TET1 has emerged as an epigenetic brake on beige fat thermogenesis via histone remodeling involving HDAC3—uncovering novel avenues to boost energy expenditure. They also discovered JMJD8 as a unique adipocyte-intrinsic regulator linking inflammation and insulin resistance, interacting with IRF3 and Perilipin 2 to drive lipid droplet hypertrophy, highlighting how intracellular metabolic cues translate into systemic effects. Furthermore, they recently identified an analogous role for JMJD8 in the liver promoting steatosis.

In skeletal muscle, their studies show that DNMT3A regulates mitochondrial function and endurance capacity, while AIFM2 controls glucose utilization in glycolytic fibers, establishing direct connections between muscle epigenetics and whole-body energy homeostasis. These findings suggest that enhancing muscle metabolism represents an exciting therapeutic avenue to improve systemic metabolic health.

Together, their research aims to provide a comprehensive understanding of the epigenetic and molecular mechanisms controlling metabolic function, with the vision of informing innovative and effective treatments for complex metabolic disorders.

Vision and Future Directions:  Their research defines epigenetic control and intrinsic cellular signaling as key regulators of metabolic regulation. They are expanding these insights into inter-organ communication, including adipose–liver crosstalk, to understand how tissue-specific factors shape systemic metabolism. This integrated approach bridges fundamental epigenetic biology and translational therapeutics, providing a framework for novel interventions to improve metabolic health and reduce cardiometabolic risk.

Research Expertise and Interest

metabolism, obesity, adipose tissue, epigenetics

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