James Pullman

TL;DR: It is found that humans and mouse models with tubulointerstitial fibrosis had lower expression of key enzymes and regulators of fatty acid oxidation (FAO) and higher intracellular lipid deposition compared to controls, raising the possibility that correcting the metabolic defect in FAO may be useful for preventing and treating chronic kidney disease.

TL;DR: The canonical complement signaling pathway was determined to be statistically differentially regulated in both DKD glomeruli and tubuli and was associated with increased glomerulosclerosis even in a different set of DKD samples.

TL;DR: It is established that epithelial injury and Notch signaling play key roles in fibrosis development and indicate that Notch blockade may be a therapeutic strategy to reduce fibrosis and ESRD development.

TL;DR: Analysis of tubular cells from patients with proliferative, membranous and mixed LN indicated pathways relevant to inflammation and fibrosis, which offer insight into their histologic differences.

TL;DR: It is demonstrated that genome-wide cytosine methylation patterns of healthy and chronic kidney disease tubule samples obtained from patients show significant differences, raising the possibility that epigenetic dysregulation plays a role in chronic kidneys disease development via influencing core pro-fibrotic pathways and can aid the development of novel biomarkers and future therapeutics.