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Our laboratory uses the combination of genetics, molecular biology, and informatics to investigate pathways underlying common cardiovascular and metabolic disorders. We exploit natural genetic variation among inbred strains of mice and among human populations to identify novel targets and formulate hypotheses, and we perform validation using experimental perturbations in mice. A major focus has been the interactions underlying commom, complex forms of atherosclerosis, heart failure, and fatty liver disease.

Our laboratory has taken advantage of high throughput biologic technologies, such as transcriptomics, metabolomics, and proteomics, to help develop new approaches to understand complex traits. We have shown that when integrated with natural genetic variation, such multi-omics analyses can be used to model biologic pathways and uncover regulatory mechanisms, an approach known as “systems genetics”. We have recently applied this to better understand host-gut microbiome interactions and how they contribute to cardio-metabolic disease.

During the past 15 years, we have developed a unique mapping approach in mice that is analogous to genome-wide association studies in humans. This approach utilizes a well-characterized population of 100 inbred strains of mice, termed the Hybrid Mouse Diversity Panel (HMDP). A major advantage of this approach is that the resolution is much better than with traditional genetic crosses. It also facilitates studies of gene-by-environment interactions, which are very difficult to address in human populations, and it has important advantages for systems-based approaches which require access to relevant tissues.

Some recent publications that are representative of our approaches are the following:

Email: jlusis@mednet.ucla.edu