Metabolic and immune responses are the most basic and important survival requirements in multicellular organisms. Recent studies by us and others have uncovered the strong mutual influence of metabolism and macrophage inflammatory responses. Identifying the underlying mechanisms is a fascinating and vibrant novel research area and its findings will be critical for the design of therapeutic treatments for both metabolic and inflammatory diseases.RESEARCH INTERESTS
Our research is focused on the mechanisms linking metabolism and macrophage polarization. Macrophages are major players in the immune system. Recent studies by us and others have uncovered the strong mutual influence of metabolism and macrophage inflammatory responses. Identifying the underlying mechanisms is critical for the design of therapeutic treatments for both metabolic and inflammatory diseases.
Our several current projects investigate the role of ATP-binding Cassette Transporter G1 (ABCG1) in macrophage polarization and inflammatory diseases. ABCG1 promotes cholesterol efflux from cells and regulates intracellular cholesterol homeostasis, which is crucial for survival and function of cells. We have recently made the novel discovery that absence of ABCG1 in macrophages inhibits tumor growth, metastasis and prolongs survival of mice through the modulation of macrophage function within the tumor. In particular, in the absence of ABCG1, the tumor-associated macrophages shift from a tumor-promoting M2 (anti-inflammatory) to a tumor-fighting M1 (proinflammatory) phenotype (Sag et al, Nature Communications, 2015).
Our goal is to (1) uncover the molecular mechanisms through which ABCG1-deficiency shifts macrophages to a tumor-fighting M1 phenotype and (2) investigate the role of ABCG1 in macrophage polarization in humans, particularly in human cancer.
Furthermore, we aim to investigate the impact of macrophage ABCG1 deficiency on other diseases in which macrophages play a key role, such as type II diabetes and obesity.