Diabetes and other metabolic disorders significantly enhance susceptibility to a range of chronic diseases including cardiovascular diseases. Common cellular mechanisms' underlying these chronic diseases includes disrupted cellular energetics and protein misfolding. Both genetic factors and lifestyle changes trigger the onset and progression of these chronic diseases. My long term research interest lies in understanding how genes and lifestyle interact in determining predisposition to chronic diseases. We recently developed Drosophila models to delay age-associated cardiac dysfunction with time-restricted feeding without affecting caloric intake. We discovered novel pathways that preserve age-associated deterioration of cardiac defects under time-restricted feeding conditions. Now we are using this non-pharmacological novel strategy to prevent cardiac defects and metabolic disorders associated with diabetes mellitus, obesity and other metabolic diseases.
We are investigating the mechanisms of laminopathiy-induced cardiac and skeletal muscle dysfunction. Laminopathies are a group of genetic disorders caused by mutations in the LMNA gene encoding A-type lamins, intermediate filaments that line the inside of the nuclear envelope. Patients with laminopathies exhibit a spectrum of phenotypes including cardiac and skeletal muscle dysfunction, dysplasia, diabetes and progeria. Among these, dilated cardiomyopathy is a major cause of death, yet the underlying mechanisms of pathology remain unknown. Our fruit fly model is a unique in vivo system, which is genetically tractable and suitable to define the cardiac and skeletal muscle pathological events associated with laminopathies.