Abstract
Glaucoma is a major cause of blindness in China and the world. Currently, all therapeutic means in treating open-angle glaucoma are limited to control the progression of optic neuropathy by lowering intraocular pressure (IOP). Clinically available medicines lower IOP by either enhancing the uveoscleral pathway or inhibiting aqueous humor production. Since the primary cause of IOP elevation in POAG is elevated outflow resistance in the trabecular outflow pathway, current medicines are not able to correct the underlying pathogenesis and pathophysiology of the disease. In this review article, we discuss a series of new therapeutic targets and therapeutic approaches that are designed to directly modify the pathological changes related to the reduction in trabecular outflow in glaucoma patients. Some of these targets and approaches may produce a significant breakthrough in the treatment of this devastating disease.
| Original language | English |
|---|---|
| Pages (from-to) | 471-475 |
| Number of pages | 5 |
| Journal | Chinese Journal of Ophthalmology |
| Volume | 52 |
| Issue number | 6 |
| DOIs | |
| State | Published - 11 Jun 2016 |
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Keywords
- Drug discovery
- Glaucoma, open-angle
- Molecular targeted therapy
- Trabecular meshwork
Cite this
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Novel therapeutic targets for reduction of intraocular pressure in primary open angle glaucoma. / Mao, Weiming; Liu, Yang; Wordinger, Robert J.; Clark, Abbot; Pang, Iok-Hou.
In: Chinese Journal of Ophthalmology, Vol. 52, No. 6, 11.06.2016, p. 471-475.Research output: Contribution to journal › Review article
TY - JOUR
T1 - Novel therapeutic targets for reduction of intraocular pressure in primary open angle glaucoma
AU - Mao, Weiming
AU - Liu, Yang
AU - Wordinger, Robert J.
AU - Clark, Abbot
AU - Pang, Iok-Hou
PY - 2016/6/11
Y1 - 2016/6/11
N2 - Glaucoma is a major cause of blindness in China and the world. Currently, all therapeutic means in treating open-angle glaucoma are limited to control the progression of optic neuropathy by lowering intraocular pressure (IOP). Clinically available medicines lower IOP by either enhancing the uveoscleral pathway or inhibiting aqueous humor production. Since the primary cause of IOP elevation in POAG is elevated outflow resistance in the trabecular outflow pathway, current medicines are not able to correct the underlying pathogenesis and pathophysiology of the disease. In this review article, we discuss a series of new therapeutic targets and therapeutic approaches that are designed to directly modify the pathological changes related to the reduction in trabecular outflow in glaucoma patients. Some of these targets and approaches may produce a significant breakthrough in the treatment of this devastating disease.
AB - Glaucoma is a major cause of blindness in China and the world. Currently, all therapeutic means in treating open-angle glaucoma are limited to control the progression of optic neuropathy by lowering intraocular pressure (IOP). Clinically available medicines lower IOP by either enhancing the uveoscleral pathway or inhibiting aqueous humor production. Since the primary cause of IOP elevation in POAG is elevated outflow resistance in the trabecular outflow pathway, current medicines are not able to correct the underlying pathogenesis and pathophysiology of the disease. In this review article, we discuss a series of new therapeutic targets and therapeutic approaches that are designed to directly modify the pathological changes related to the reduction in trabecular outflow in glaucoma patients. Some of these targets and approaches may produce a significant breakthrough in the treatment of this devastating disease.
KW - Drug discovery
KW - Glaucoma, open-angle
KW - Molecular targeted therapy
KW - Trabecular meshwork
UR - http://www.scopus.com/inward/record.url?scp=84986212683&partnerID=8YFLogxK
U2 - 10.3760/cma.j.issn.0412-4081.2016.06.019
DO - 10.3760/cma.j.issn.0412-4081.2016.06.019
M3 - Review article
C2 - 27373575
AN - SCOPUS:84986212683
VL - 52
SP - 471
EP - 475
JO - Chinese Journal of Ophthalmology
JF - Chinese Journal of Ophthalmology
SN - 0412-4081
IS - 6
ER -