We are studying the role of advanced glycation endproducts (AGE) and oxidative stress in podocyte injury and diabetic kidney disease. We are studying the role and the post-translational regulation (acetylation) of key transcription factors such as FOXO, NF-kB and Stat3 in mediating podocyte injury and diabetic kidney disease.

We are studying the signaling network that mediates podocyte differentiation and injury using both in vitro and in vivo models. We are studying the relationship between mechanical force, morphology, and chemical signals and their role in maintaining normal podocyte differentiation status. We are studying the mechanism of podocyte injury in diabetic kidney disease and HIV-associated nephropathy. We are studying how retinoic acid could repair podocyte injury through induction of differentiation and regeneration process.

We are studying the role of HIV viral protein in the development of HIV-associated nephropathy. The role and signaling pathways of HIV Nef have been studied in kidney podocytes. We are also investigating the mechanism of chronic HIV infection on the progression of other kidney diseases such as diabetic nephropathy and hypertensive kidney disease.

We are using systems biology approach to study cell signaling and gene transcription networks in kidney disease. We are studying the transcriptome, epigenome and proteome in injured podocytes and diseased kidney. We are using systems pharmacology approach to identify new drug targets or therapy for kidney disease.

We have identified that HIPK2 plays a key role in kidney fibrosis. We are studying the mechanism of HIPK2 in mediating kidney fibrosis and try to identify potential anti-fibrosis therapy by targeting HIPK2. Please visit the He Laboratory.