The kidney undergoes injury as a common complication of infection, surgical procedures, medications, and systemic disease. Once injured, the kidney’s ability to return to its prior state of function is unfortunately compromised. The result is progressive and irreversible chronic kidney disease which at minimum require lifelong monitoring for systemic effects and at worse, results in end-stage kidney disease requiring dialysis or kidney transplant. Supportive measures only slow the progression of chronic kidney disease and currently, there is no treatment resulting in the functional repair of injured kidney tissue.
In collaboration with Dr. Mark Majesky & Dr. David Beier, our current projects focus on the role of histone modifications in the regulation of gene expression for models of kidney injury. Epigenetic regulation of transcription through the posttranslational modification of histones plays an important role in any situation where cells undergo transitional states. We investigate the proteomic, genetic and epigenetic changes that in the setting of kidney injury and repair with the goal of identifying mechanisms by which the response to kidney injury can be redirected from fibrosis to functional organ tissue.