THERAPEUTIC TARGETS FOR GLAUCOMA

被引:2
作者
Sorbera, L. A. [1 ]
Aravamudan, J. [1 ]
Dulsat, C. [1 ]
Rosa, E. [1 ]
机构
[1] Thomson Reuters, Barcelona 08025, Spain
关键词
CARBONIC-ANHYDRASE INHIBITORS; OPEN-ANGLE GLAUCOMA; CALCIUM-CHANNEL BLOCKER; OCULAR BLOOD-FLOW; INTRAOCULAR-PRESSURE; VISUAL FUNCTION; RECEPTOR; PROTECTION; SYSTEM; CELLS;
D O I
10.1358/dof.2010.035.07.1520867
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Glaucoma is a group of progressive optic neuropathies that involves the death of retinal ganglion cells, the consequent deformation of the optic nerve head and a progressive reduction in the visual field. The disease can be associated with elevated intraocular pressure (IOP) due to accumulation of aqueous humor. The buildup of aqueous fluid compresses the nerve fibers of the optic nerve, leading to damage and loss of vision. There is no cure for glaucoma, although the condition can be managed through reduction of IOP. In general, existing pharmacotherapy consists of improving the flow or reducing the production of intraocular fluid. Available agents include miotics, beta-blockers, carbonic anhydrase inhibitors, prostaglandin analogues and alpha(2)-adrenoceptor agonists. However, the search continues for more effective treatment strategies for glaucoma, with investigation focusing on identifying novel targets for therapeutic intervention. This article presents those drug targets that are currently under active investigation for the treatment of glaucoma.
引用
收藏
页码:585 / 592
页数:8
相关论文
共 63 条
[1]   Corneal Neovascularization and Ocular Irritancy Responses in Dogs Following Topical Ocular Administration of an EP4-Prostaglandin E2 Agonist [J].
Aguirre, Shirley A. ;
Huang, Wenhu ;
Prasanna, Ganesh ;
Jessen, Bart .
TOXICOLOGIC PATHOLOGY, 2009, 37 (07) :911-920
[2]  
Aihara M, 2010, CLIN OPHTHALMOL, V4, P163
[3]   Axonal transport and cytoskeletal changes in the laminar regions after elevated intraocular pressure [J].
Balaratnasingam, Chandrakumar ;
Morgan, William H. ;
Bass, Louise ;
Matich, Graeme ;
Cringle, Stephen J. ;
Yu, Dao-Yi .
INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE, 2007, 48 (08) :3632-3644
[4]   Blood Pressure, Perfusion Pressure, and Glaucoma [J].
Caprioli, Joseph ;
Coleman, Anne L. .
AMERICAN JOURNAL OF OPHTHALMOLOGY, 2010, 149 (05) :704-712
[5]   Epidemiology of primary glaucoma: prevalence, incidence, and blinding effects [J].
Cedrone, Claudio ;
Mancino, Raffaele ;
Cerulli, Angelica ;
Cesareo, Massimo ;
Nucci, Carlo .
GLAUCOMA: AN OPEN WINDOW TO NEURODEGENERATION AND NEUROPROTECTION, 2008, 173 :3-14
[6]  
Challa Pratap, 2008, Int Ophthalmol Clin, V48, P73, DOI 10.1097/IIO.0b013e318187e71a
[7]  
Chen L, 2009, MOL VIS, V15, P1664
[8]   KR-31378, a Potassium-Channel Opener, Induces the Protection of Retinal Ganglion Cells in Rat Retinal Ischemic Models [J].
Choi, Anho ;
Choi, Jun-Sub ;
Yoon, Yone-Jung ;
Kim, Kyung-A ;
Joo, Choun-Ki .
JOURNAL OF PHARMACOLOGICAL SCIENCES, 2009, 109 (04) :511-517
[9]  
Collison DJ, 2000, INVEST OPHTH VIS SCI, V41, P2633
[10]   Pharmacotherapy of intraocular pressure - part II. Carbonic anhydrase inhibitors, prostaglandin analogues and prostamides [J].
Costagliola, Ciro ;
dell'Omo, Roberto ;
Romano, Mario R. ;
Rinaldi, Michele ;
Zeppa, Lucia ;
Parmeggiani, Francesco .
EXPERT OPINION ON PHARMACOTHERAPY, 2009, 10 (17) :2859-2870