The Schelling laboratory utilizes in vitro molecular and cellular methods, animal models and human samples to investigate glomerular and tubulointerstitial pathophysiology in the context of CKD, especially diabetic kidney disease. We made the initial discovery that proximal tubule cell apoptosis leads to tubular atrophy, which strongly predicts CKD progression. We have continued to build on that theme, with many publications that characterize the cellular pathways that impact on tubular epithelial cell survival, most recently the role of filtered fatty acid uptake by fatty acid transporter-2 (FATP2) in proximal tubule glucolipotoxicity. We are actively pursuing projects which explore the pathophysiology of FATP2-mediated cytotoxicity, as well as the development of FATP2 inhibitors as a potential treatment for diabetes and diabetic kidney disease.
|Major Research Areas|
|Apoptosis, Biochemical Pathways, Cell Death Mechanisms, Chronic kidney disease, Development of Therapeutics, Drug discovery, Membrane Protein Expression/Function, Membrane Transport, Mitochondrial biology and pathology, Protein Structure/Function, Renal Proximal Tubules, Therapeutics|
|Animal Models, Biochemistry, Cellular Biology, Drug discovery , Metabolism|
|Chronic kidney disease, Diabetes|
|Cell Culture, Cellular and Molecular Biology, Confocal Microscopy, FRET, Gel Electrophoresis/Western Blots, Immunohistochemistry, In-vivo Animal Models, Molecular Biology, Protein Chemistry, Protein Expression, Quantitative Fluorescence Imaging, Quantitative RT-PCR, RNA Isolation and Gene Expression Analysis, RT-PCR|