Assistant professor,Albert Einstein College of Medicine,USA
Dr Gao has more than 16 years of experience in biology and is the author of more than 11 scientific publications. Following a Ph.D. in genetics at Fudan University, Shanghai, China, he first took up a postdoc research fellow position at The Children?s Hospital Boston and Harvard Medical School, then associate scientist at Columbia University Medical Center, Assistant professor at Mount Sinai School of Medicine, and currently Albert Einstein College of Medicine. As an experienced molecular, cellular and in vivo biologist, he has been focusing on studies of early kidney development and kidney disease since 2001. Currently the major interest of Dr Gao?s research is to identify novel mechanisms of kidney injury occurring in HIV-positive persons and use in vitro and murine models to generate new strategies to prevent and treat kidney diseases.
Despite the success of antiretroviral therapy (ART) in improving mortality, HIV-infected persons remain at increased risk of death. Kidney disease is an important contributor to mortality in HIV-infected patients and HIV-associated nephropathy (HIVAN) is the most common cause of end stage renal disease (ESRD) in HIV-infected persons. Though ART is effective in reducing the severity of HIVAN, the incidence of ESRD due to HIVAN has not decreased appreciably. Moreover, there is an unexplained paradox regarding the pathogenesis and treatment of HIVAN. In vitro and in vivo models demonstrate that expression of HIV-1 Vpr and Nef in renal epithelial cells (in the absence of viral replication) is a key mediator of HIVAN pathogenesis. However, current ART agents act by suppressing HIV replication via inhibition of proteins encoded by the viral pol and env genes and are not known to directly target the function of Vpr or Nef. In addition, recent research has shown that HIV-1 protease inhibitors (PI) are effective in treating HIV-negative patients with steroid-dependent nephrotic syndrome, raising the question whether ART exerts salutary effects in HIVAN via mechanisms that are independent of suppression of HIV replication. HIV infection also increases the risk of progression of non-HIVAN kidney diseases, including diabetic nephropathy, yet it is unknown whether ART retards progression of non-HIVAN forms of CKD. Since the prevalence of diabetes mellitus is increasing among HIV-infected persons, it is crucial that we improve our understanding of the effects of ART on diabetes-induced kidney injury in the setting of HIV infection.
Our long-term goal is to understand the mechanisms by which HIV infection predisposes patients to CKD to facilitate development of novel strategies to prevent and treat kidney disease in this vulnerable population. The major focus of research in our laboratory is to identify novel mechanisms of kidney injury occurring in HIV-positive persons and we use in vitro and murine models to generate new strategies to prevent and treat kidney diseases.