Prof. Ge-Zhi Xu

Principal Investigator

Research Directions
Possible link between neural gial cell activation and neuronal apoptosis in retinal degeneration diseases and diabetic retinopathy
Contact  Information
Address: Eye Ear Nose and Throat Hospital of Fudan University, 83 Fen Yang Road, Shanghai 200433, China
Tel:86-021-64318258  Fax: 021-64377134-706 Email:xugezhi@sohu.com

Dr. Ge-Zhi Xu graduated from Academy of Chinese University of Hong Kong and received MD in ophthalmology in 1995. He is the leader of Retinal Group of Shanghai Association of Ophthalmology. He is a member of Ocular Fundus Group of Chinese Association of Ophthalmology, and American Society of Retina Specialists. He has been inviting as a member of Editorial Board in Chinese Journal of Ophthalmology, Chinese Journal of Ocular Fundus Diseases, etc. He has won a number of awards including Progress Reward of National Education Committee, Progress Reward of Health Ministry of China, and Progress Reward of Science and Technology Committee of Shanghai Municipality.


Enrollment Major

Research Direction

Possible link between neural gial cell activation and neuronal apoptosis in retinal degeneration diseases and diabetic retinopathy


Research Work
In the outer retinal degeneration diseases, such as age-related macular degeneration (AMD), retinitis pigmentosa (RP) and pathological myopia, apoptosis is the common pathway in which photoreceptors die. It is awfully difficult to treat these diseases at present, because the pathogenic factors are not fully understood and there is little to do to reconstruct the RPE-Bruch Membrane-Choroidal capillary complex.
In the review of past researches, most studies neglected to explore the possible effect that sicken retinal neural cells might have on the progression of photoreceptor apoptosis. For example, could the apoptosis of photoreceptor itself be one of deteriorating factors? In the progression of photoreceptor apoptosis, what are the changes of other retinal neural cells? And what effect could these changes impose on the disease progression? Could there be some treatments deriving from modulation on these changes?
During recent years, our research group has done some work concerning retinal glial cells under pathologic status, which might, to some extent, answer those questions mentioned above.
1.    Morphologic and functional changes of retinal microglia in light-induced photoreceptor degeneration.

2.    Microglial morphology and function-related molecular in diabetic rats

3.    Alterations of Müller cells under pathologic status and its role in retinal diseases


Selected Publications

  1. Qin YW, Zhu MJ, Qu XM, Xu GZ*, Yu YF, Witt RE, Wang WJ (2010). Regional macular light sensitivity changes in myopic Chinese adults: a micro perimetry 1 study. Invest Ophthalmol Vis Sci, 51: 4451-4457

  2. Ye XF, Xu GZ*, Chang Q, Fan JW, Sun ZC, Qin YW, Jiang AC (2010). ERK1/2 signaling pathways involved in VEGF release in diabetic rat retina. Invest Ophthalmol Vis Sci, 51: 5266-5233

  3. Ni YQ, Xu GZ*, Hu WZ, Shi L, Qin YW, Da CD (2008). Naloxone has neuroprotective effects against light-induced photoreceptor degeneration through inhibiting retinal microglia activation. Invest Ophthalmol Vis Sci, 49: 2589-2598

  4. Ni YQ, Gan DK, Xu HD, Xu GZ*, Da CD (2009). Neuroprotective effect of transcorneal electrical stimulation on light-induced photoreceptor degeneration. Exp Neurol, 220: 410-411

  5. Qin YW,Xu GZ*,Wang WJ (2006). Dendritic abnormalities in retinal ganglion cells of three-month diabetic rats. Curr Eye Res, 31: 967-974

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