He has had a long-standing interest in various aspects of cellular injury and repair mechanisms in the kidney with a special emphasis on the role of inflammation, biomarkers and stem cells.
His team has a great deal of experience with various animal models of AKI and chronic kidney disease and their work has been cited more than 43,500 times. He has a citation h-index of 109 and has received two MERIT awards from NIH and serves on NIH Council.
The team have extended their repair and stem cell work to creation of induced pluripotent stem (iPS) cells and the development of an approach to differentiate iPS and embryonic stem cells to cells of the kidney lineage. They published the first demonstration of creation of an iPS cell line from a kidney disease, polycystic kidney disease, which has an abnormality with plausible significance with respect to the etiology of the disease. iPS cells generated from fibroblasts of humans with autosomal dominant PKD had reduced ciliary levels of polycystin-2 which could be rescued in iPS-derived hepatoblasts by overexpression of polycystin-1.
This work opened up the possibility to conduct “kidney clinical trials in a dish” with patient specific cells that can by evaluated for efficacy of potential therapeutic agents. They also recently reported a rapid and efficient process, derived by techniques guided by principles of kidney development, by which human iPS and ES cells can be differentiated into intermediate mesoderm and subsequently form multisegmented kidney structures containing podocalyxin expressing cell clusters surrounded by a epithelial layer mimicking Bowman’s capsule, flowing into a continuous tubular structure with properties of proximal tubule, followed by loop of Henle and distal convoluted tubule.