Diabetic retinopathy: could the alpha-1 antitrypsin be a therapeutic option?

Diabetic retinopathy is one of the most important causes of blindness. The underlying mechanisms of this disease include inflammatory changes and remodeling processes of the extracellular-matrix (ECM) leading to pericyte and vascular endothelial cell damage that affects the retinal circulation. In t...

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Autores principales:	Ortiz,Gustavo, Salica,Juan P, Chuluyan,Eduardo H, Gallo,Juan E
Lenguaje:	English
Publicado:	Sociedad de Biología de Chile 2014
Materias:	Diabetic retinopathy Alpha-1-antitrypsin Diabetes Endogenous anti-inflammatory agents Retinal inflammation NF-kB
Acceso en línea:	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602014000100052
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spelling	oai:scielo:S0716-976020140001000522015-10-30Diabetic retinopathy: could the alpha-1 antitrypsin be a therapeutic option?Ortiz,GustavoSalica,Juan PChuluyan,Eduardo HGallo,Juan E Diabetic retinopathy Alpha-1-antitrypsin Diabetes Endogenous anti-inflammatory agents Retinal inflammation NF-kB Diabetic retinopathy is one of the most important causes of blindness. The underlying mechanisms of this disease include inflammatory changes and remodeling processes of the extracellular-matrix (ECM) leading to pericyte and vascular endothelial cell damage that affects the retinal circulation. In turn, this causes hypoxia leading to release of vascular endothelial growth factor (VEGF) to induce the angiogenesis process. Alpha-1 antitrypsin (AAT) is the most important circulating inhibitor of serine proteases (SERPIN). Its targets include elastase, plasmin, thrombin, trypsin, chymotrypsin, proteinase 3 (PR-3) and plasminogen activator (PAI). AAT modulates the effect of protease-activated receptors (PARs) during inflammatory responses. Plasma levels of AAT can increase 4-fold during acute inflammation then is so-called acute phase protein (APPs). Individuals with low serum levels of AAT could develop disease in lung, liver and pancreas. AAT is involved in extracellular matrix remodeling and inflammation, particularly migration and chemotaxis of neutrophils. It can also suppress nitric oxide (NO) by nitric oxide sintase (NOS) inhibition. AAT binds their targets in an irreversible way resulting in product degradation. The aim of this review is to focus on the points of contact between multiple factors involved in diabetic retinopathy and AAT resembling pleiotropic effects that might be beneficial.info:eu-repo/semantics/openAccessSociedad de Biología de ChileBiological Research v.47 20142014-01-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602014000100052en10.1186/0717-6287-47-58
institution	Scielo Chile
collection	Scielo Chile
language	English
topic	Diabetic retinopathy Alpha-1-antitrypsin Diabetes Endogenous anti-inflammatory agents Retinal inflammation NF-kB
spellingShingle	Diabetic retinopathy Alpha-1-antitrypsin Diabetes Endogenous anti-inflammatory agents Retinal inflammation NF-kB Ortiz,Gustavo Salica,Juan P Chuluyan,Eduardo H Gallo,Juan E Diabetic retinopathy: could the alpha-1 antitrypsin be a therapeutic option?
description	Diabetic retinopathy is one of the most important causes of blindness. The underlying mechanisms of this disease include inflammatory changes and remodeling processes of the extracellular-matrix (ECM) leading to pericyte and vascular endothelial cell damage that affects the retinal circulation. In turn, this causes hypoxia leading to release of vascular endothelial growth factor (VEGF) to induce the angiogenesis process. Alpha-1 antitrypsin (AAT) is the most important circulating inhibitor of serine proteases (SERPIN). Its targets include elastase, plasmin, thrombin, trypsin, chymotrypsin, proteinase 3 (PR-3) and plasminogen activator (PAI). AAT modulates the effect of protease-activated receptors (PARs) during inflammatory responses. Plasma levels of AAT can increase 4-fold during acute inflammation then is so-called acute phase protein (APPs). Individuals with low serum levels of AAT could develop disease in lung, liver and pancreas. AAT is involved in extracellular matrix remodeling and inflammation, particularly migration and chemotaxis of neutrophils. It can also suppress nitric oxide (NO) by nitric oxide sintase (NOS) inhibition. AAT binds their targets in an irreversible way resulting in product degradation. The aim of this review is to focus on the points of contact between multiple factors involved in diabetic retinopathy and AAT resembling pleiotropic effects that might be beneficial.
author	Ortiz,Gustavo Salica,Juan P Chuluyan,Eduardo H Gallo,Juan E
author_facet	Ortiz,Gustavo Salica,Juan P Chuluyan,Eduardo H Gallo,Juan E
author_sort	Ortiz,Gustavo
title	Diabetic retinopathy: could the alpha-1 antitrypsin be a therapeutic option?
title_short	Diabetic retinopathy: could the alpha-1 antitrypsin be a therapeutic option?
title_full	Diabetic retinopathy: could the alpha-1 antitrypsin be a therapeutic option?
title_fullStr	Diabetic retinopathy: could the alpha-1 antitrypsin be a therapeutic option?
title_full_unstemmed	Diabetic retinopathy: could the alpha-1 antitrypsin be a therapeutic option?
title_sort	diabetic retinopathy: could the alpha-1 antitrypsin be a therapeutic option?
publisher	Sociedad de Biología de Chile
publishDate	2014
url	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0716-97602014000100052
work_keys_str_mv	AT ortizgustavo diabeticretinopathycouldthealpha1antitrypsinbeatherapeuticoption AT salicajuanp diabeticretinopathycouldthealpha1antitrypsinbeatherapeuticoption AT chuluyaneduardoh diabeticretinopathycouldthealpha1antitrypsinbeatherapeuticoption AT gallojuane diabeticretinopathycouldthealpha1antitrypsinbeatherapeuticoption
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Diabetic retinopathy: could the alpha-1 antitrypsin be a therapeutic option?

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