Welcome to the Huang Research Lab
Chronic kidney disease (CKD) is a global disaster disease. Regarding the underlying disorder, CKD is generally characterized by progressive inflammation and fibrosis of the kidney, and ultimately leading to end stage of renal disease (ESRD). My laboratory has a long-term interest in understanding mechanisms of fibrogenesis underlying CKD and developing potential therapeutic interventions for this disease.
One current project in the lab is to use our newly discovered small molecule, KH-3/KH-39, to evaluate mRNA-binding protein HuR-targeted therapeutics for inhibition of renal fibrosis by using CKD animal models. Human antigen R (HuR), a mRNA-binding protein, has been identified as a key modulator in immune response and inflammation through regulating mRNA stability of cytokines, inflammatory factors, and proteins critical for these events. Enhanced renal cellular HuR translocation and activation has been observed in varied kidney diseases in both patients and animal models. Therefore, selective inhibition of HuR function in diseased kidney represents a promising strategy for the treatment of renal inflammation and subsequent progression of CKD. A second project in the lab investigates the role of the EphB2 receptor tyrosine kinase as a new previously unexplored central player in CKD that is involved in mediating both inflammatory and fibrotic events. In a third project, we are investigating roles of the nicotinamide N-methyl transferase (NNMT) related pathways and the cGMP deficiency in the progression of diabetic nephropathy by using the type 2 diabetic db/db mouse model, since NNMT is a top upregulated gene in human CKD kidney including DKD, where it is associated with tubulointerstitial damage and rapid disease progression, and cGMP deficiency contributes to the progression of CKD through both hemodynamic and pro-fibrotic effects. Our goal is to do research that will help solve the CKD problems and move the promising new findings into the clinic to benefit patients.