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Acute Kidney Injury

 BASIC SCIENCE

chronic kidney diseasediabetic nephropathydevelopmentmatrix biology, hypertension, integrin biology,  growth factorseicosanoid biologygene deliveryendothelial cell biologybioartificial kidney


                              acute kidney injury

 

VCKD researchers are using a variety of experimental approaches to understand the underlying mechanisms of kidney injury and repair and the development novel therapies to reduce injury and enhance these intrinsic repair mechanisms. These studes are highly complementary to the clinical research studies into the genetics, biomarkers and outcomes in patients presenting to the hospital with AKI that are also being conducted through the VCKD. In the long run it is anticipated that close collaborative interactions between the basic and clinical VCKD scientists involved in AKI  research will lead to streamlining and clinical development of drug candidates to ameliorate the disease burden in patients with AKI.

Director

 

Members

The de Caestecker lab is using small molecule screens to identify and optimize novel therapeutics to enhance normal repair after AKI. Our long term goals are to understand the molecular pathways regulating these responses, and to develop therapeutics to prevent long term adverse sequelae of AKI on renal fibrosis. He is also interested in developing and disseminating best practice protocols for AKI studies in rodents both through the annual Vanderbilt Mouse Kidney Injury Workshop which he coordinates each summer, and through open dissemination of techniques and protocols to the nephrology community as a whole.

The Gewin lab is looking at the role of the TGF-beta superfamily in acute kidney injury (AKI) and the progression of AKI to chronic kidney disease. To investigate this, rodent models of AKI are performed on genetically modified mice and complemented with in vitro studies using proximal tubule epithelial cells.

The Haase lab is interested in the role oxygen and energy metabolism in renal repair and regeneration following ischemic re-perfusion injury.  The lab uses state-of-the-art genetic, biochemical, mass spectrometry and metabolomic approaches to study the role of hypoxia-inducible factors in the regulation of epithelial and vascular repair of the injury kidney.

The Harris Lab is interested in the mechanisms of repair and regeneration after acute kidney injury. Areas of ongoing research include the role of epidermal growth factor receptor signaling in epithelial repair and the role of renal macrophages and dendritic cells in orchestrating recovery from AKI.

Our laboratory uses state of the art transgenic mice, cell biology and biochemistry to define how cell-extracellular matrix interactions modulate susceptiblity of the kidney to injury and its recovery after injury.

The Zhang Lab is interested in the mechanisms of repair and regeneration after acute kidney injury and particularly in the roles of macrophages/dendritic cells in incomplete recovery from AKI which lead to CKD.