The Gewin lab investigates tubular responses to kidney injury and how these responses can modulate repair versus continued injury and fibrosis. Injured tubules are potent producers of growth factors (e.g. TGF-beta and Wnt/beta-catenin) that affect both tubular and paracrine (e.g. fibroblast, macrophage) responses to kidney injury. Recently, the Gewin lab has also been interested in understanding how changes in cell cycle and metabolism of the injured tubules, especially the proximal tubule, affect the response to injury. Uninjured proximal tubules are quiescent and preferentially use fatty acid oxidation to generate the large amount of energy necessary to support their reabsorptive functions. After injury, there are significant changes to cell cycle and metabolism, but whether these changes are adaptive or maladaptive remains unclear. 

The Gewin lab has a number of projects looking at the basic science mechanisms underlying kidney injury and fibrosis. These involve both exposure to in vitro techniques, genetic mouse models of injury, and single cell/single nuclear RNA sequencing techniques.