My lab investigates the mechanisms of acute kidney injury (AKI) in animal models of renal ischemia- reperfusion and sepsis. In particular, we study the interplay between tubular apoptosis, inflammation, metabolism and innate immunity in shaping the renal response to injury and therapy. We have identified guanine nucleotides, p53, macrophage subsets and Toll-like receptors as major modulators of the injury process, metabolism and tubular cross-talk as well as the post injury outcome and response to therapy.
Research: Complication of Diabetes and Obesity
Keywords:
- Oxidative Stress
- Progressive Chronic Kidney Disease
- Quantitative Microscopy
- Cell Biology of Acute Kidney Injury