Our laboratory explores the contribution of the immune system and inflammatory mediators to the progression of target organ damage in the setting of cardiovascular disease. We are pursuing several related projects in this field:
(1) The actions of type 1 angiotensin receptors on specific immune cell populations in hypertension, target organ damage, and tissue fibrosis.
(2) Cell-specific actions of inflammatory cytokines in regulating blood pressure and end-organ injury.
(3) Mechanism through which dendritic cells regulate renal sodium reabsorption.
(4) The contributions of Wnt O-acylation to kidney scar formation.
Education and Training
- Fellow in Nephrology, Medicine, Duke University, 2001 - 2003
- Chief Medical Resident, Medicine, Duke University, 2000 - 2001
- Fellow in Nephrology, Medicine, Duke University, 1999 - 2000
- Medical Resident, Medicine, Duke University, 1996 - 1999
- M.D., Duke University, 1996
- The Role of the IL-1 Receptor in the AKI to CKD transition
- The interleukin-1 receptor regulates crosstalk between myeloid and renal tubular cells in hypertension
- Duke Training Grant in Nephrology
- The interleukin-1 receptor modulates blood pressure and renal tubular injury
- IPA extenstion - Robert Griffiths
- Role of Dendritic Cell-mediated T Cell Activation in Salt-sensitive Hypertension
- Dendritic cells activate pro-hypertensive T cells to drive sodium reaborption in kidney
- Tissue-specific generation of tumour necrosis factor-a contributes to the pathogenesis of hypertension