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LETTER TO THE EDITOR |
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Year : 2008 | Volume
: 56
| Issue : 3 | Page : 255-256 |
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Debate on the various anti-vascular endothelial growth factor drugs
Mohammad Reza Khalili, Hamid Hosseini
Department of Ophthalmology, Poostchi Eye Research Center, Shiraz University of Medical Sciences, Iran
Date of Web Publication | 22-Apr-2008 |
Correspondence Address: Hamid Hosseini Department of Ophthalmology, Poostchi Eye Research Center, Shiraz University of Medical Sciences Iran
Source of Support: None, Conflict of Interest: None | Check |
DOI: 10.4103/0301-4738.40375
How to cite this article: Khalili MR, Hosseini H. Debate on the various anti-vascular endothelial growth factor drugs. Indian J Ophthalmol 2008;56:255-6 |
Dear Editor,
We read with interest the article "A comparative debate on the various anti-vascular endothelial growth factor drugs: Pegaptanib sodium (Macugen), ranibizumab (Lucentis) and bevacizumab (Avastin)" by Nagpal et al . [1]
Herein, we demonstrate another potentially useful aspect of pegaptanib sodium in comparison with ranibizumab and bevacizumab, not mentioned in the above article.
Vascular endothelial growth factor-A (VEGF-A) has been recognized as an important neuroprotectant in the central nervous system. [2],[3] Receptors for VEGF-A are also present in normal retinal neuronal cells, [4],[5] indicating a possible functional role for VEGF-A in the neural retina. Recently, Nishijama et al. demonstrated that VEGF-A is a survival factor for retinal neurons and a critical neuroprotectant during the adaptive response to ischemic injury. [6] Perhaps, the most surprising finding in their study concerned the reliance of normal retinal ganglion cells (RGCs) on VEGF-A for survival. Through both direct quantification of RGC numbers and assessment of optic nerve axon viability, they observed a dose-dependent decrease in neuron numbers after VEGF depletion with an antibody that blocks all VEGF isoforms. Interestingly, when the effects of VEGF were blocked with pegaptanib, which binds to VEGF164 and does not bind to VEGF120, there was no decrease in retinal RGC viability. VEGF164-treated eyes after ischemia showed obvious signs of disseminated intraretinal hemorrhages, suggesting an increase in vascular leakage caused by the VEGF164 treatment whereas no retinal hemorrhage was detected in the VEGF120-treated eyes. [6] To conclude, the use of selective anti-VEGF agents such as pegaptanib, which inhibits pathologic VEGF164 and spares all other VEGF isomers, is strongly recommended to preserve retinal neurons in the long term, especially in the context of ischemic retinal diseases.
References | | |
1. | Nagpal M, Nagpal K, Nagpal PN. A comparative debate on the various anti-vascular endothelial growth factor drugs: Pegaptanib sodium (Macugen), ranibizumab (Lucentis) and bevacizumab (Avastin). Indian J Ophthalmol 2007;55:437-9. [ PUBMED] |
2. | Storkebaum E, Lambrechts D, Carmeliet P. VEGF: Once regarded as a specific angiogenic factor, now implicated in neuroprotection. Bioessays 2004;26:943-54. [ PUBMED] [ FULLTEXT] |
3. | Sun Y, Jin K, Xie L, Childs J, Mao XO, Logvinova A, Greenberg DA. VEGF-induced neuroprotection, neurogenesis and angiogenesis after focal cerebral ischemia. J Clin Invest 2003;111:1843-51. [ PUBMED] [ FULLTEXT] |
4. | Kim I, Ryan AM, Rohan R, Amano S, Agular S, Miller JW, et al . Constitutive expression of VEGF, VEGFR-1 and VEGFR-2 in normal eyes. Invest Ophthalmol Vis Sci 1999;40:2115-21. [ PUBMED] [ FULLTEXT] |
5. | Yang X, Cepko CL. Flk-1, a receptor for vascular endothelial growth factor (VEGF), is expressed by retinal progenitor cells. J Neurosci 1996;16:6089-99. [ PUBMED] [ FULLTEXT] |
6. | Nishijima K, Ng YS, Zhong L, Bradley J, Schubert W, Jo N, et al . Vascular endothelial growth factor: A is a survival factor for retinal neurons and a critical neuroprotectant during the adaptive response to ischemic injury. Am J Pathol 2007;171:53-67. [ PUBMED] [ FULLTEXT] |
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