My group focuses on the role of pathogenic fibroblasts, which can be recruited from fat (adipose) tissue in the context of obesity, type-2 diabetes, muscle degeneration, and cancer. We are also interested in adipocyte heterogeneity and mechanisms controlling fatty acid transport in the context of type-2 diabetes and cancer. White and brown adipocytes are continuously replaced as they undergo senescence, and their pools in fat tissue are maintained by adipose stem cells (ASCs). In obesity, ASCs over-proliferate and undergo replicative senescence, hence, aggravating aging. This was revealed by our studies in mice lacking telomerase in ASCs. Currently, we are testing the role of replicative senescence in other types of stem cells and the effects on aging-associated neurological and muscular dysfunction. We have discovered that, in chronic disease, tissues recruit ASCs, which can fuel cancer chemoresistance and metastasis, as well as fibrosis. Taking advantage of our expertise in targeted therapeutics, we have developed the first experimental drug targeting ASCs. Our publications demonstrate that this drug prevents obesity and suppresses cancer progression in mice. We have also applied ablation of ASC as a new therapeutic approach to muscular dystrophy intervention. We have also reported a panel of peptides that can be used for non-invasive detection and imaging of metastatic cancer cells and their conversion to therapeutics blocking cancer progression.
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