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, which is an independent risk factor for hypertension and cardiovascular disease. Renal proximal tubule epithelial cells (PTCs) are vital to the function of the kidney and integral to the pathology of the injured kidney, because they are the most sensitive kidney cell type to ischemia and nephrotoxic insults. The overall goal of Dr. Brooks’ 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, he has uncovered a significant role of mitochondria in PTC cell death. He was the first to demonstrate pathological mitochondrial fragmentation in PTCs during kidney injury leading to cell death (Brooks et al. JCI 2009) and the therapeutic potential of inhibiting mitochondrial fragmentation using small molecule inhibitors. He also demonstrated a direct interaction between Bcl-2 family proteins and mitochondrial morphology proteins (Brooks et al. PNAS 2007). In addition, he has identified an important role of PTCs in regulating inflammatory processes during AKI. He 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 autophagic regulation of immune processes in AKI, determining if the activation of novel G2/M arrest regulators following AKI contributes to fibrosis, and investigating whether blocking formation of the TOR-autophagy spatial coupling compartment (associated with pro-secretory cells) contributes to fibrosis in injured kidneys.