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      ¿Reducen las estatinas el riesgo de glaucoma? revisión de las evidencias Translated title: Do statins reduce the risk of glaucoma? review of the evidences

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          Abstract

          Resumen Introducción: Los objetivos de este trabajo son revisar y resumir los datos publicados hasta el momento que relacionen el uso de estatinas con el riesgo de aparición o de agravamiento de glaucoma y plantear una hipótesis que explique los efectos protectores de las estatinas y su asociación con un menor riesgo de glaucoma. Método: se realizó una revisión en PubMed usando los términos "statins, hmg coa" o "hmg coa inhibitors" y "glaucoma" o "open angle glaucoma" o "intraocular pressure". Se seleccionaron todos los artículos que incluían estudios clínicos o meta-análisis y se excluyeron comentarios, cartas a editor, artículos retractados e investigación en modelos animales. Todos los artículos fueron posteriores a 2004. Se emplearon en la revisión 17 artículos. Resultados: la mayor parte de los estudios muestran un efecto protector de las estatinas frente a la aparición y agravamiento del glaucoma de ángulo abierto. Sin embargo, otros estudios no llegan a encontrar una relación significativa e incluso alguno muestra una relación entre el glaucoma y el empleo de estatinas a altas dosis. Los efectos neuroprotectores y la inhibición de la Rho-quinasa podrían explicar los efectos encontrados. Conclusiones: la evidencia publicada no es suficiente como para recomendar el tratamiento con estatinas con el objetivo de prevenir el avance o la aparición del glaucoma.

          Translated abstract

          Abstract Introduction: The objectives of this article are to review and summarize the updated published data that show the relation between treatment with statins and the incidence and progression of glaucoma. We also aimed to pose a hypothesis to explain the protective effects of statins and its association with glaucoma risk. Method: a review of the literature was carried out in the PubMed database considering the MeSH terms "statins, hmg coa" or "hmg coa inhibitors" and "glaucoma" or "open angle glaucoma" or "intraocular pressure". All articles including clinical studies and meta-analysis were selected. Comments, letters to editors, retracted articles and research on animal models were excluded. All the articles were published from 2004. 17 articles were finally selected for review. Results: most of the studies showed a protective effect of statins on incidence or progression of open angle glaucoma. Nevertheless, other studies did not find a significant association and even one study found association between statin treatment at high doses and more incidence of glaucoma. Neuroprotective effects of statin and inhibition of Rho-kinase may help explain the described effects. Conclusions: The published results are not enough evidence to support statin recommendation as preventive treatment for the incidence or progression of glaucoma.

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          Most cited references32

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          Global prevalence of glaucoma and projections of glaucoma burden through 2040: a systematic review and meta-analysis.

          Glaucoma is the leading cause of global irreversible blindness. Present estimates of global glaucoma prevalence are not up-to-date and focused mainly on European ancestry populations. We systematically examined the global prevalence of primary open-angle glaucoma (POAG) and primary angle-closure glaucoma (PACG), and projected the number of affected people in 2020 and 2040. Systematic review and meta-analysis. Data from 50 population-based studies (3770 POAG cases among 140,496 examined individuals and 786 PACG cases among 112 398 examined individuals). We searched PubMed, Medline, and Web of Science for population-based studies of glaucoma prevalence published up to March 25, 2013. Hierarchical Bayesian approach was used to estimate the pooled glaucoma prevalence of the population aged 40-80 years along with 95% credible intervals (CrIs). Projections of glaucoma were estimated based on the United Nations World Population Prospects. Bayesian meta-regression models were performed to assess the association between the prevalence of POAG and the relevant factors. Prevalence and projection numbers of glaucoma cases. The global prevalence of glaucoma for population aged 40-80 years is 3.54% (95% CrI, 2.09-5.82). The prevalence of POAG is highest in Africa (4.20%; 95% CrI, 2.08-7.35), and the prevalence of PACG is highest in Asia (1.09%; 95% CrI, 0.43-2.32). In 2013, the number of people (aged 40-80 years) with glaucoma worldwide was estimated to be 64.3 million, increasing to 76.0 million in 2020 and 111.8 million in 2040. In the Bayesian meta-regression model, men were more likely to have POAG than women (odds ratio [OR], 1.36; 95% CrI, 1.23-1.52), and after adjusting for age, gender, habitation type, response rate, and year of study, people of African ancestry were more likely to have POAG than people of European ancestry (OR, 2.80; 95% CrI, 1.83-4.06), and people living in urban areas were more likely to have POAG than those in rural areas (OR, 1.58; 95% CrI, 1.19-2.04). The number of people with glaucoma worldwide will increase to 111.8 million in 2040, disproportionally affecting people residing in Asia and Africa. These estimates are important in guiding the designs of glaucoma screening, treatment, and related public health strategies. Copyright © 2014 American Academy of Ophthalmology. Published by Elsevier Inc. All rights reserved.
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            Modulation of aqueous humor outflow facility by the Rho kinase-specific inhibitor Y-27632.

            The goal of this study was to investigate the role of Rho kinase in the modulation of aqueous humor outflow facility. Rho kinase, a critical downstream effector of Rho GTPase is recognized to control the formation of actin stress fibers, focal adhesions, and cellular contraction. Expression of Rho GTPase, Rho kinase, and other downstream targets of Rho GTPase were determined in human trabecular meshwork (HTM) and Schlemm's canal (SC) primary cell cultures by Western blot analysis. The Rho kinase-specific inhibitor (Y-27632)-induced changes in actin stress fibers, focal adhesions, and protein phosphotyrosine status were evaluated by staining with rhodamine-phalloidin, anti-paxillin, and anti-phosphotyrosine antibodies, respectively. Myosin light-chain phosphorylation was determined by Western blot analysis. Y-27632-induced changes in SC cell monolayer permeability were quantitated using a colorimetric assay to evaluate horseradish peroxidase diffusion through SC cell monolayers grown in transwell chambers. Aqueous humor outflow facility was measured using enucleated porcine eyes and a constant-pressure perfusion system. Treatment of HTM and SC cells with Y-27632 (10 microM) led to significant but reversible changes in cell shape and decreases in actin stress fibers, focal adhesions, and protein phosphotyrosine staining. SC cell monolayer permeability increased (by 80%) in response to Y-27632 (10 microM) treatment, whereas myosin light-chain phosphorylation was decreased in both HTM and SC cells. Aqueous humor outflow facility increased (40%-80%) in enucleated porcine eyes perfused with Y-27632 (10-100 microM), and this effect was associated with widening of the extracellular spaces, particularly the optically empty area of the juxtacanalicular tissue (JCT). The integrity of inner wall of aqueous plexi, however, was observed to be intact. Based on the Rho kinase inhibitor-induced changes in myosin light-chain phosphorylation and actomyosin organization, it is reasonable to conclude that cellular relaxation and loss of cell-substratum adhesions in HTM and SC cells could result in either increased paracellular fluid flow across Schlemm's canal or altered flow pathway through the JCT, thereby lowering resistance to outflow. This study also suggests Rho kinase as a potential therapeutic target for the development of drugs to modulate intraocular pressure in glaucoma patients.
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              Neuroprotective effects of atorvastatin against glutamate-induced excitotoxicity in primary cortical neurones.

              Statins [3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors] exert cholesterol-independent pleiotropic effects that include anti-thrombotic, anti-inflammatory, and anti-oxidative properties. Here, we examined direct protective effects of atorvastatin on neurones in different cell damage models in vitro. Primary cortical neurones were pre-treated with atorvastatin and then exposed to (i) glutamate, (ii) oxygen-glucose deprivation or (iii) several apoptosis-inducing compounds. Atorvastatin significantly protected from glutamate-induced excitotoxicity as evidenced by propidium iodide staining, nuclear morphology, release of lactate dehydrogenase, and mitochondrial tetrazolium metabolism, but not from oxygen-glucose deprivation or apoptotic cell death. This anti-excitototoxic effect was evident with 2-4 days pre-treatment but not with daily administration or shorter-term pre-treatment. The protective properties occurred independently of 3-hydroxy-3-methylglutaryl-CoA reductase inhibition because co-treatment with mevalonate or other isoprenoids did not reverse or attenuate neuroprotection. Atorvastatin attenuated the glutamate-induced increase of intracellular calcium, which was associated with a modulation of NMDA receptor function. Taken together, atorvastatin exerts specific anti-excitotoxic effects independent of 3-hydroxy-3-methylglutaryl-CoA reductase inhibition, which has potential therapeutic implications.
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                Author and article information

                Journal
                ars
                Ars Pharmaceutica (Internet)
                Ars Pharm
                Universidad de Granada (Granada, Granada, Spain )
                2340-9894
                December 2021
                : 62
                : 4
                : 419-437
                Affiliations
                [1] Sevilla Andalucía orgnameUniversidad de Sevilla orgdiv1Facultad de Farmacia orgdiv2Departamento Farmacología Spain
                Article
                S2340-98942021000400419 S2340-9894(21)06200400419
                10.30827/ars.v62i4.21463
                4efa931f-2e8f-4064-999b-a4c5bb233cd2

                This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.

                History
                : 02 September 2021
                : 04 June 2021
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 32, Pages: 19
                Product

                SciELO Spain

                Categories
                Artículos de Revisión

                estatinas,glaucoma,hmg coa inhibitors,statins,inhibidores HMG-Coenzima A

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