Diabetic retinopathy: could the alpha-1 antitrypsin be a therapeutic option?
- Autores
- Ortiz, Gustavo Alfredo; Salica, Juan Pablo; Chuluyan, Hector Eduardo; Gallo, Juan Eduardo Maria
- Año de publicación
- 2014
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- 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.
Fil: Ortiz, Gustavo Alfredo. Universidad Austral. Facultad de Ciencias Biomédicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Salica, Juan Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Austral. Facultad de Ciencias Biomédicas; Argentina
Fil: Chuluyan, Hector Eduardo. Universidad de Buenos Aires. Facultad de Medicina; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
Fil: Gallo, Juan Eduardo Maria. Universidad Austral. Facultad de Ciencias Biomédicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina - Materia
-
Diabetes
Diabetic Retinopathy
Alpha-1-Antitrypsin
Retinal Inflammation - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/31796
Ver los metadatos del registro completo
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Diabetic retinopathy: could the alpha-1 antitrypsin be a therapeutic option?Ortiz, Gustavo AlfredoSalica, Juan PabloChuluyan, Hector EduardoGallo, Juan Eduardo MariaDiabetesDiabetic RetinopathyAlpha-1-AntitrypsinRetinal Inflammationhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3https://purl.org/becyt/ford/3.4https://purl.org/becyt/ford/3https://purl.org/becyt/ford/3.2https://purl.org/becyt/ford/3Diabetic 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.Fil: Ortiz, Gustavo Alfredo. Universidad Austral. Facultad de Ciencias Biomédicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Salica, Juan Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Austral. Facultad de Ciencias Biomédicas; ArgentinaFil: Chuluyan, Hector Eduardo. Universidad de Buenos Aires. Facultad de Medicina; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: Gallo, Juan Eduardo Maria. Universidad Austral. Facultad de Ciencias Biomédicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaBioMed Central2014-11info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/31796Ortiz, Gustavo Alfredo; Salica, Juan Pablo; Chuluyan, Hector Eduardo; Gallo, Juan Eduardo Maria; Diabetic retinopathy: could the alpha-1 antitrypsin be a therapeutic option?; BioMed Central; Biological Research; 47; 11-2014; 58-670716-97600717-6287CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4335423/info:eu-repo/semantics/altIdentifier/doi/10.1186/0717-6287-47-58info:eu-repo/semantics/altIdentifier/url/https://biolres.biomedcentral.com/articles/10.1186/0717-6287-47-58info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-15T14:49:29Zoai:ri.conicet.gov.ar:11336/31796instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-10-15 14:49:30.064CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
Diabetic retinopathy: could the alpha-1 antitrypsin be a therapeutic option? |
title |
Diabetic retinopathy: could the alpha-1 antitrypsin be a therapeutic option? |
spellingShingle |
Diabetic retinopathy: could the alpha-1 antitrypsin be a therapeutic option? Ortiz, Gustavo Alfredo Diabetes Diabetic Retinopathy Alpha-1-Antitrypsin Retinal Inflammation |
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? |
dc.creator.none.fl_str_mv |
Ortiz, Gustavo Alfredo Salica, Juan Pablo Chuluyan, Hector Eduardo Gallo, Juan Eduardo Maria |
author |
Ortiz, Gustavo Alfredo |
author_facet |
Ortiz, Gustavo Alfredo Salica, Juan Pablo Chuluyan, Hector Eduardo Gallo, Juan Eduardo Maria |
author_role |
author |
author2 |
Salica, Juan Pablo Chuluyan, Hector Eduardo Gallo, Juan Eduardo Maria |
author2_role |
author author author |
dc.subject.none.fl_str_mv |
Diabetes Diabetic Retinopathy Alpha-1-Antitrypsin Retinal Inflammation |
topic |
Diabetes Diabetic Retinopathy Alpha-1-Antitrypsin Retinal Inflammation |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3 https://purl.org/becyt/ford/3.4 https://purl.org/becyt/ford/3 https://purl.org/becyt/ford/3.2 https://purl.org/becyt/ford/3 |
dc.description.none.fl_txt_mv |
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. Fil: Ortiz, Gustavo Alfredo. Universidad Austral. Facultad de Ciencias Biomédicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Salica, Juan Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Austral. Facultad de Ciencias Biomédicas; Argentina Fil: Chuluyan, Hector Eduardo. Universidad de Buenos Aires. Facultad de Medicina; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Gallo, Juan Eduardo Maria. Universidad Austral. Facultad de Ciencias Biomédicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina |
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. |
publishDate |
2014 |
dc.date.none.fl_str_mv |
2014-11 |
dc.type.none.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo |
format |
article |
status_str |
publishedVersion |
dc.identifier.none.fl_str_mv |
http://hdl.handle.net/11336/31796 Ortiz, Gustavo Alfredo; Salica, Juan Pablo; Chuluyan, Hector Eduardo; Gallo, Juan Eduardo Maria; Diabetic retinopathy: could the alpha-1 antitrypsin be a therapeutic option?; BioMed Central; Biological Research; 47; 11-2014; 58-67 0716-9760 0717-6287 CONICET Digital CONICET |
url |
http://hdl.handle.net/11336/31796 |
identifier_str_mv |
Ortiz, Gustavo Alfredo; Salica, Juan Pablo; Chuluyan, Hector Eduardo; Gallo, Juan Eduardo Maria; Diabetic retinopathy: could the alpha-1 antitrypsin be a therapeutic option?; BioMed Central; Biological Research; 47; 11-2014; 58-67 0716-9760 0717-6287 CONICET Digital CONICET |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
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dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by/2.5/ar/ |
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openAccess |
rights_invalid_str_mv |
https://creativecommons.org/licenses/by/2.5/ar/ |
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application/pdf application/pdf application/pdf application/pdf application/pdf |
dc.publisher.none.fl_str_mv |
BioMed Central |
publisher.none.fl_str_mv |
BioMed Central |
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reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas |
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Consejo Nacional de Investigaciones Científicas y Técnicas |
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CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas |
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dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
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