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INVITED REVIEW
Year : 2014  |  Volume : 9  |  Issue : 16  |  Page : 1502-1505

Efficacy of granulocyte-colony stimulating factor treatment in a rat model of anterior ischemic optic neuropathy


1 Department of Molecular Biology and Human Genetics, Tzu Chi University, Hualien 97002, Taiwan, China
2 Institute of Eye Research, Buddhist Tzu Chi General Hospital; Institute of Medical Sciences, Tzu Chi University, Hualien 97002, Taiwan, China

Correspondence Address:
Rong-Kung Tsai
Institute of Eye Research, Buddhist Tzu Chi General Hospital, Tzu Chi University, No. 707, Sec. 3, Chung-Yang Rd, Hualien, 97002, Taiwan
China
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Source of Support: This work was funded by a National Science Council Grant from the Taiwanese Government NSC100-2314-B-303-005., Conflict of Interest: None


DOI: 10.4103/1673-5374.139472

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Non-arteritic anterior ischemic optic neuropathy (NA-AION) is the most common cause of acute ischemic damage to the optic nerve (ON), and the leading cause of seriously impaired vision in people over 55 years of age. It demonstrated that subcutaneous administration of Granulocyte colony-stimulating factor (G-CSF) reduces RGC death in an ON crush model in rats, and that the neuroprotective effects may involve both anti-apoptotic and anti-inflammatory processes. Our recent work shows that the protective actions of G-CSF in rAION models may involve both anti-apoptotic and anti-inflammatory processes. However, the exact rescuing mechanisms involved in the administration of G-CSF in rAION models need further investigation. In addition, further studies on the administration of G-CSF at different time intervals after the induction of rAION may be able to illustrate whether treatment given at a later time is still neuroprotective. Further, it is unknown whether treatment using G-CSF combined with other drugs will result in a synergistic effect in a rAION model. Inflammation induced by ischemia plays an essential role on the ON head in NA-AION, which can result in disc edema and compartment changes. Therefore, it is reasonable that adding an anti-inflammatory drug may enhance the therapeutic effects of G-CSF. An ongoing goal is to evaluate the novel sites of action of both G-CSF and other anti-inflammatory drugs, and to identify the functionally protective pathways to enhance RGC survival. These investigations may open up new therapeutic avenues for the treatment of ischemic optic neuropathy.


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