Acute Kidney Injury
Acute kidney injury (AKI) occurs in nearly 1 of 5 hospitalized patients and is associated with increased morbidity and mortality across all ages. Many AKI patients will recover kidney function post-injury but then progress to chronic kidney disease (CKD). The mechanisms are poorly understood and there are currently no effective therapies to prevent, limit, or reverse the tissue damage. There is a critical need to identify mechanisms involved in the pathogenesis of AKI. Our long-term goal is to elucidate these mechanisms and leverage them for new therapies to limit AKI and prevent the transition to CKD. We have two major projects that are currently be investigated: 1. Sirtuin 5 mediated protection against AKI and 2. Mir17~92 in the renal endothelium during AKI. We are in the process of designing pre-clinical studies to test whether both these mechanisms can be leveraged to protect against AKI.
Maternal Environment and Kidney Formation
The maternal environment is critical to not only the health of the fetus but also the health and development of the kidney. Alterations in the maternal environment can lead to drastic changes in the development of the kidney and lead to congenital kidney abnormalities. We have two major projects that are currently be investigated: 1. The role of maternal diabetes on kidney formation and 2. Low protein diet and kidney formation.
VHL Mutations and Kidney Cancer
VHL (the major regulator of HIFs) is a tumor suppressor protein, which is a protein upon mutation causes tumorigenesis and cancer development, with the kidney as one of the primary sites. Loss of VHL plays a prominent role in the pathogenesis of clear cell renal cell carcinoma (ccRCC), and up to 70% of all ccRCC cases are attributed to VHL gene defects. We have one major project that is currently be investigated: 1. The development of ccRCC cancer models.