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Craig brooks Ph.D.

Department: Vanderbilt Center for Kidney Disease

Biography

Acute kidney injury (AKI) occurs in ~13% of hospitalized patients and is associated with a fourfold increase in mortality. AKI also predisposes patients to chronic kidney disease. AKI also predisposes patients to chronic kidney disease (CKD), which affects ~10% of the world's population. Renal proximal tubule epithelial cells (PTCs) are vital to the function of the kidney and are also integral to the pathology of the injured kidney, as the most sensitive kidney cell type to ischemia and nephrotoxic insults. The overall goal of my research is to delineate the molecular mechanisms of PTC cell injury/death, survival and subsequent regeneration to identify therapeutic targets to treat AKI. To this end, I investigated mechanisms of PTC cell death. I was the first to demonstrate pathological mitochondrial fragmentation in PTCs during kidney injury, leading to cell death, (Brooks et al. JCI 2009) and demonstrate the therapeutic potential of inhibiting mitochondrial fragmentation using small molecule inhibitors. I also demonstrated a direct interaction between Bcl-2 family proteins and mitochondrial morphology proteins (Brooks et al., PNAS, 2007; Brooks et al., AJP Cell 2011). Next, I focused on the role of PTCs in regulating inflammatory processes during AKI. I found tubular cell phagocytosis suppressed inflammation (Yang, Brooks et al., J. Clinical Inv., 2015) as well as induced autophagy, which in turn, inhibited proximal tubular cell activation of T cells through MHC presentation (Brooks et al., EMBO, 2015). Current research interests include: Further delineating the mechanism and therapeutic potential of autophagy activation in the regulation of immune processes in AKI; Determining if the activation of novel cell cycle regulators following AKI contributes to fibrosis and chronic kidney disease through induction of mTOR-LC3 associated pro-secretory phenotype; and examining if mitochondrial dynamics proteins, such as mitofusins, modulate autophagic flux in AKI.

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