Chronic low-grade inflammation is a common feature of many diseases including diabetes, and cardiovascular diseases. These disorders in part characterized by dysregulated innate immune responses and metabolic changes in the cells. Growing evidence indicates that cellular metabolism not only provide ATP and biosynthetic precursors for cell activities but also play a crucial role in controlling immunity and inflammation. This suggests that changes in metabolic programming including aerobic glycolysis, oxidative phosphorylation, fatty acid and cholesterol synthesis in immune (and even non-immune) cells tightly regulates their functions and shapes the cell fate. Consequently, metabolic reprogramming can have a significant impact on the progression and resolution of inflammation. Recent studies have revealed activating certain transcription factors such as LXRs modulated cell metabolism by inducing lipid synthesis or accumulation of immunometabolites like acetyl-CoA, which serve as signal transducers to develop an inflammatory phenotype, the new concept known as innate immune memory. Cell metabolism is intricately linked to epigenetic profile of the cells, which together establish non-specific innate immune memory and heightened responses to a secondary stimulus.

Our main scientific interest involved studying metabolic and epigenetic changes regulating inflammatory and anti-inflammatory responses of the cells in the context of cardiovascular diseases. We are also interested to define how modulation of metabolic pathway affects progression or resolution of inflammation. We are particularly interested in investigating lipid metabolism and cholesterol synthesis pathways and the role of LXRs and SREBPs in regulation of inflammation. Ultimate goal is to use the data to suggest an immunomodulatory therapeutic tool for inflammatory diseases associated with atherosclerosis.