Current and emerging medical therapies in the treatment of glaucoma

Bagnis, Alessandro; Papadia, Marina; Scotto, Riccardo; Traverso, Carlo Enrico

doi:10.1517/14728214.2011.563733

Cited by 33 publications

(41 citation statements)

References 63 publications

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“…Elevated levels of IOP due to incorrect aqueous humor drainage are considered to be the main cause of RGC apoptosis; however, damage to RGCs is also observed in patients with normal IOP values (7).…”

Section: Pathogenesis Of Glaucomamentioning

confidence: 99%

“…However, a number of side-effects have been reported following administration of these drugs (7). In addition, the inconvenience of treatment protocols involving multiple daily administration has led to poor compliance and has been widely discussed as a common issue for glaucoma patients (13,14).…”

Section: Current Treatments For Glaucomamentioning

confidence: 99%

“…There are five main classes of topical ocular hypotensive drugs: i) β-adrenergic antagonists (β-blockers), including timolol, which may reduce IOP by 22-25% (15). Patients with glaucoma are generally older and may have cardiac or pulmonary disease, which may be worsened following the use of β-blockers (7). In addition, ocular side-effects that occur with the use of β-blockers include burning, stinging and dry eyes, and are generally associated with preservatives in the drug solution (16,17).…”

Section: Current Treatments For Glaucomamentioning

confidence: 99%

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Targeting the A3 adenosine receptor for glaucoma treatment (Review)

Fishman

Cohen

Bar-Yehuda

2013

Molecular Medicine Reports

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Abstract. Glaucoma is a worldwide disease and the second leading cause of blindness. Current treatments are associated with a number of side-effects and poor compliance, due to the requirement for treatment administration several times a day. These treatments typically aim to lower intraocular pressure (IOP); however, they are unable to protect retinal ganglion cells (RGCs) from undergoing apoptosis, which is the main cause of vision loss. A 3 adenosine receptor (A 3 AR) agonists have been found to protect normal cells from undergoing apoptosis via the downregulation of death signals. Furthermore, A 3 AR agonists have been reported to have several ophthalmological effects, including the prevention of ganglion cell apoptosis in vitro and in vivo and anti-inflammatory effects in experimental models of autoimmune uveitis. CF101, an orally bioavailable A 3 AR agonist, has been analyzed in dry eye syndrome phase II clinical trials and was identified to be safe and well tolerated. The anti-inflammatory effect of CF101 was shown to significantly improve corneal staining, tear meniscus and tear break-up time in dry eye patients. In addition, CF101 was found to decrease IOP in patients. The safety and efficacy of CF101, together with its suitability for oral administration, indicates that it has potential as a candidate drug for the treatment of glaucoma.

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Section: Pathogenesis Of Glaucomamentioning

confidence: 99%

Section: Current Treatments For Glaucomamentioning

confidence: 99%

Section: Current Treatments For Glaucomamentioning

confidence: 99%

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Targeting the A3 adenosine receptor for glaucoma treatment (Review)

Fishman

Cohen

Bar-Yehuda

2013

Molecular Medicine Reports

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“…La muerte de las neuronas de la retina es el punto común final entre el glaucoma y la enfermedad de la retina 5 . Como tal, las terapias hipotensoras y neuroprotectoras son una necesidad terapéutica imprescindible para los pacientes que padecen esta enfermedad 6 . A pesar de los esfuerzos e investigaciones en el campo del glaucoma, su fisiopatología aun no ha sido totalmente esclarecida.…”

Section: Introductionunclassified

Comparación de dos modelos experimentales de glaucoma en conejos

Tártara¹,

Leavi²,

Campana³

et al. 2018

Rev Fac Cien Med Univ Nac Cordoba

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. Resumen:Objetivo: comparar dos modelos de glaucoma experimental por inducción de hipertensión ocular en conejos y describir cambios anatomo-patológicos. Materiales y métodos: Se utilizaron 16 conejos New Zealand, hembras, de 2-3 kg. Modelo A (n=6): cauterización de venas epiesclerales y perilimbares en ojo derecho (OD) con cauterio eléctrico quirúrgico. Modelo B (n=10): inyección intracamerular en OD de α-quimotripsina. Se midió la presión intraocular (PIO) antes y después de la inducción de la hipertensión ocular (HTO), una vez por semana, a la misma hora del día, durante 40 días, con tonómetro manual. Los animales fueron sacrificados por inhalación de CO 2 . En ambos modelos la PIO del ojo izquierdo (OI).fue tomado como valor control. La media y error estándar (EE) de los valores de la PIO, expresada en mmHg, fueron evaluadas y comparadas estadísticamente aplicando Test T de Student considerando un nivel de significación de p < 0.05. Resultados: La PIO en OI (control) del modelo A: fue 12,9±1,05 y en el modelo B: 12,9±1,09. No se observaron diferencias significativas entre ambas. Modelo A: el aumento de la PIO en OD fue 14,7% (14,8±1,4) con respecto a OI. Se observó un incremento significativo de la PIO dentro de las primeras 24 hs: 23,5±1,9 (p<0,05) comparado con el valor del ojo control. No hubo diferencias significativas con los controles posteriores. Modelo B: el aumento de la PIO en OD fue 129,1% (29,6±3,4) con respecto al OI. En todos los casos se observó un incremento desde el día 1 (p<0,05). El pico de PIO en OD se evidenció el día 25: 35±3,4 (p<0,05). El incremento de la PIO inducida en el modelo B fue significativamente mayor (p<0,01) que en el modelo A. En ambos modelos hubo pérdida de células ganglionares de la retina, pero sólo en el modelo B se observaron los siguientes cambios anatomo-patológicos: buftalmus, subluxación del cristalino y aumento de la excavación de la papila. Conclusión: De acuerdo a este estudio, el modelo B aparece como el método más apropiado a los fines de inducir un incremento rápido y controlado de la IOP en conejos y más importante, este incremento sería capaz de mantenerse alto a lo largo de periodos de tiempos extendidos. Este modelo podría ser de gran utilidad para evaluar la eficacia de nuevos sistemas oculares de liberación de fármacos y realizar futuros estudios de la fisiopatología del glaucoma. Palabras clave: modelo experimental de glaucoma; α-quimotripsina; cauterización de las venas epiesclerales; hipertensión ocular. Abstract:Objective: to compare two models of experimental glaucoma by induction of ocular hypertension in rabbits. Materials and methods: Sixteen New Zealand female rabbits, 2-3 kg were used. Model A (n=6): cauterization of episcleral and perilimbar veins of the right eye (RE) with surgical electrocautery. Model B (n=10): Injection of α-chymotrypsin in posterior chamber of RE. Intraocular pressure (IOP) was measured before and after the induction of ocular hypertension (OHT), once a week at the same time of day for 40 days, with a manual tonomete...

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“…2,[6][7][8][9] Although several different drugs are currently available for lowering IOP, the efficacy of available drugs is not adequate to control elevated IOP to the desired levels in different glaucoma patients. [10][11][12] Therefore, there is an immediate unmet need for novel and targeted therapy to effectively manage elevated IOP and prevent loss of vision in glaucoma patients. To develop novel IOP-lowering treatments, however, it is imperative that we identify the external cues and unravel different intracellular pathways which regulate IOP and understand the molecular basis of increased IOP.…”

Section: Introductionmentioning

confidence: 99%

Bioactive Lysophospholipids: Role in Regulation of Aqueous Humor Outflow and Intraocular Pressure in the Context of Pathobiology and Therapy of Glaucoma

Rao

2014

Journal of Ocular Pharmacology and Therapeutics

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Homeostasis of aqueous humor (AH) outflow and intraocular pressure (IOP) is essential for normal vision. Impaired AH outflow through the trabecular meshwork (TM) and a resultant elevation in IOP are common changes in primary open-angle glaucoma (POAG), which is the most prevalent form of glaucoma. Although elevated IOP has been recognized as a definitive risk factor for POAG and lowering elevated IOP remains a mainstay for glaucoma treatment, little is known about the molecular mechanisms, especially external cues and intracellular pathways, involved in the regulation of AH outflow in both normal and glaucomatous eyes. In addition, despite the recognition that increased resistance to AH outflow via the conventional pathway consisting of TM and Schlemm's canal is the main cause for elevated IOP, there are no clinically approved drugs that target the conventional pathway to lower IOP in glaucoma patients. The aim of this article is to briefly review published work on the importance of bioactive lysophospholipids (eg, lysophosphatidic acid and sphingosine-1-phosphate), their receptors, metabolism, signaling, and role in the regulation of AH outflow via the TM and IOP, and to discuss pharmacological targeting of key proteins in the lysophospholipid signaling pathways to lower IOP in glaucoma patients.

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Current and emerging medical therapies in the treatment of glaucoma

Cited by 33 publications

References 63 publications

Targeting the A3 adenosine receptor for glaucoma treatment (Review)

Targeting the A3 adenosine receptor for glaucoma treatment (Review)

Comparación de dos modelos experimentales de glaucoma en conejos

Bioactive Lysophospholipids: Role in Regulation of Aqueous Humor Outflow and Intraocular Pressure in the Context of Pathobiology and Therapy of Glaucoma

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