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Prof Dave Shima
Institute of Ophthalmology
11-43 Bath Street
London
EC1V 9EL
Tel: 020 76084069
Fax: 020 76084060
Appointment
  • Rothes Professor of Preventive Ophthalmology
  • Inst Ophthalmology - Ocular Biology
  • Institute of Ophthalmology
  • Faculty of Brain Sciences
Research Groups
Research Summary
Age-related macular degeneration (AMD) and diabetic retinopathy (DR) are the leading causes of blindness in the middle-aged and elderly, together afflicting well over 25 million patients in the US and EU. 1.4 million Americans over the age of 55, and a similar number in the EU, will develop advanced AMD over the next 5 years, characterized by severe vision loss or blindness. Similarly, more than 5 million diabetics currently suffer sight-threatening complications associated with the more advanced stages of diabetic retinopathy. Both of these diseases are characterized by abnormalities in the inflammatory response, neuropathy/neural cell loss and vascular growth and dysfunction.

The research aim of the team is to develop strategies for the future diagnosis and treatment of neuro-vascular ocular disease. The research strategy is based on a multi-disciplinary approach, combining basic science and more translational research; an approach which ensures rigorous exploration of disease mechanisms coupled with collaborative efforts to transform scientific data into safe, targeted and effective treatments.

Objective 1. Investigate the actions of Vascular Endothelial Growth Factor (VEGF), and VEGF antagonists on neural development, neuroprotection, inflammation and ocular neovascularisation with the aim of better defining the risk/benefit of anti-VEGF blockade in AMD, DR and other neurodegenerations

VEGF is a key intercellular signal responsible for virtually all blood vessel growth; both desirable and well regulated growth, such as during the reproductive cycle and wound healing, and abnormal growth in tumors and the ocular setting. VEGF also regulates cell function, both beneficially as it maintains the non-thrombogenic surface of vessels and promotes neuroprotection in the CNS, or detrimentally, as it triggers edema and inflammation. The fact that VEGF plays essential roles in both health and disease poses a challenge to current and future therapeutic strategies. For example, VEGF antagonists have some limitations for use in oncology, as serious side effects such as stroke, bleeding and myocardial infarction are not uncommon. An outstanding scientific problem in the field is defining the many functions of VEGF and understanding how the multiple functions of VEGF are regulated. Addressing this problem will help us to develop the next generation of anti-VEGFs that better target undesired actions of VEGF whilst preserving its beneficial functions.


My laboratory has previously identified novel functions for VEGF that have a bearing on its role as a therapeutic target. First, we demonstrated that the VEGF164 isoform, working through a receptor termed Neuropilin-1 (Nrp-1), is responsible for motor neuron migration in the developing hindbrain. This finding may be related to recent knowledge that depressed levels of VEGF in the CNS in both mice and humans is associated with an increased risk of the motor neuron disease amyotrophic lateral sclerosis. Next, we explored whether VEGF could act as a neuroprotectant in the adult retina, and demonstrated an essential role of VEGF for survival of retinal neurons during ischemia-reperfusion injuryĆ¢?"findings that have relevance for the planned use of anti-VEGFs for ischemic retinal disease such as DR and neovascular glaucoma. Our future efforts are aimed at determining if VEGF has a neuroprotective role in models of DR and glaucoma, and also trying to define the signals VEGF transmits to neurons that result in survival.

Academic Background
1995 PhD Doctor of Philosophy – Cell and Developmental Biology Harvard University
1990 BSc Bachelor of Science – Molecular Genetics Ohio State University
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