The emerging role of autophagy in the pathophysiology of diabetes mellitus
- Autores
- Gonzalez, Claudio D.; Lee, Myung Shik; Marchetti, Piero; Pietropaolo, Massimo; Towns, Roberto; Vaccaro, Maria Ines; Watada, Hirotaka; Wiley, John W.
- Año de publicación
- 2011
- Idioma
- inglés
- Tipo de recurso
- artículo
- Estado
- versión publicada
- Descripción
- An emerging body of evidence supports a role for autophagy in the pathophysiology of type 1 and type 2 diabetes mellitus. Persistent high concentrations of glucose lead to imbalances in the antioxidant capacity within the cell resulting in oxidative stress-mediated injury in both disorders. An anticipated consequence of impaired autophagy is the accumulation of dysfunctional organelles such as mitochondria within the cell. Mitochondria are the primary site of the production of reactive oxygen species (ROS), and an imbalance in ROS production relative to the cytoprotective action of autophagy may lead to the accumulation of ROS. Impaired mitochondrial function associated with increased ROS levels have been proposed as mechanisms contributing to insulin resistance. In this article we review and interpret the literature that implicates a role for autophagy in the pathophysiology of type 1 and type 2 diabetes mellitus as it applies to β-cell dysfunction, and more broadly to organ systems involved in complications of diabetes including the cardiovascular, renal and nervous systems.
Fil: Gonzalez, Claudio D.. Hospital CEMIC; Argentina. Universidad de Buenos Aires; Argentina
Fil: Lee, Myung Shik. Samsung Medical Center; Corea del Sur
Fil: Marchetti, Piero. Universita Degli Studi Di Pisa; Italia
Fil: Pietropaolo, Massimo. University Of Michigan; Estados Unidos
Fil: Towns, Roberto. University Of Michigan; Estados Unidos
Fil: Vaccaro, Maria Ines. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina
Fil: Watada, Hirotaka. Juntendo University. School of Medicine; Japón
Fil: Wiley, John W.. University Of Michigan; Estados Unidos - Materia
-
Autophagy
Diabetes Mellitus
Diabetes Complications
Oxidative Stress
Mitochondria Dysfunction
Autoimmunity - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
- Repositorio
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/13194
Ver los metadatos del registro completo
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The emerging role of autophagy in the pathophysiology of diabetes mellitusGonzalez, Claudio D.Lee, Myung ShikMarchetti, PieroPietropaolo, MassimoTowns, RobertoVaccaro, Maria InesWatada, HirotakaWiley, John W.AutophagyDiabetes MellitusDiabetes ComplicationsOxidative StressMitochondria DysfunctionAutoimmunityhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3An emerging body of evidence supports a role for autophagy in the pathophysiology of type 1 and type 2 diabetes mellitus. Persistent high concentrations of glucose lead to imbalances in the antioxidant capacity within the cell resulting in oxidative stress-mediated injury in both disorders. An anticipated consequence of impaired autophagy is the accumulation of dysfunctional organelles such as mitochondria within the cell. Mitochondria are the primary site of the production of reactive oxygen species (ROS), and an imbalance in ROS production relative to the cytoprotective action of autophagy may lead to the accumulation of ROS. Impaired mitochondrial function associated with increased ROS levels have been proposed as mechanisms contributing to insulin resistance. In this article we review and interpret the literature that implicates a role for autophagy in the pathophysiology of type 1 and type 2 diabetes mellitus as it applies to β-cell dysfunction, and more broadly to organ systems involved in complications of diabetes including the cardiovascular, renal and nervous systems.Fil: Gonzalez, Claudio D.. Hospital CEMIC; Argentina. Universidad de Buenos Aires; ArgentinaFil: Lee, Myung Shik. Samsung Medical Center; Corea del SurFil: Marchetti, Piero. Universita Degli Studi Di Pisa; ItaliaFil: Pietropaolo, Massimo. University Of Michigan; Estados UnidosFil: Towns, Roberto. University Of Michigan; Estados UnidosFil: Vaccaro, Maria Ines. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; ArgentinaFil: Watada, Hirotaka. Juntendo University. School of Medicine; JapónFil: Wiley, John W.. University Of Michigan; Estados UnidosLandes Bioscience2011-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/13194Gonzalez, Claudio D.; Lee, Myung Shik; Marchetti, Piero; Pietropaolo, Massimo; Towns, Roberto; et al.; The emerging role of autophagy in the pathophysiology of diabetes mellitus; Landes Bioscience; Autophagy; 7; 1; 1-2011; 2-111554-8627enginfo:eu-repo/semantics/altIdentifier/doi/10.4161/auto.7.1.13044info:eu-repo/semantics/altIdentifier/url/http://www.tandfonline.com/doi/abs/10.4161/auto.7.1.13044info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:44:07Zoai:ri.conicet.gov.ar:11336/13194instacron: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:34982025-09-03 09:44:07.747CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse |
dc.title.none.fl_str_mv |
The emerging role of autophagy in the pathophysiology of diabetes mellitus |
title |
The emerging role of autophagy in the pathophysiology of diabetes mellitus |
spellingShingle |
The emerging role of autophagy in the pathophysiology of diabetes mellitus Gonzalez, Claudio D. Autophagy Diabetes Mellitus Diabetes Complications Oxidative Stress Mitochondria Dysfunction Autoimmunity |
title_short |
The emerging role of autophagy in the pathophysiology of diabetes mellitus |
title_full |
The emerging role of autophagy in the pathophysiology of diabetes mellitus |
title_fullStr |
The emerging role of autophagy in the pathophysiology of diabetes mellitus |
title_full_unstemmed |
The emerging role of autophagy in the pathophysiology of diabetes mellitus |
title_sort |
The emerging role of autophagy in the pathophysiology of diabetes mellitus |
dc.creator.none.fl_str_mv |
Gonzalez, Claudio D. Lee, Myung Shik Marchetti, Piero Pietropaolo, Massimo Towns, Roberto Vaccaro, Maria Ines Watada, Hirotaka Wiley, John W. |
author |
Gonzalez, Claudio D. |
author_facet |
Gonzalez, Claudio D. Lee, Myung Shik Marchetti, Piero Pietropaolo, Massimo Towns, Roberto Vaccaro, Maria Ines Watada, Hirotaka Wiley, John W. |
author_role |
author |
author2 |
Lee, Myung Shik Marchetti, Piero Pietropaolo, Massimo Towns, Roberto Vaccaro, Maria Ines Watada, Hirotaka Wiley, John W. |
author2_role |
author author author author author author author |
dc.subject.none.fl_str_mv |
Autophagy Diabetes Mellitus Diabetes Complications Oxidative Stress Mitochondria Dysfunction Autoimmunity |
topic |
Autophagy Diabetes Mellitus Diabetes Complications Oxidative Stress Mitochondria Dysfunction Autoimmunity |
purl_subject.fl_str_mv |
https://purl.org/becyt/ford/3.1 https://purl.org/becyt/ford/3 |
dc.description.none.fl_txt_mv |
An emerging body of evidence supports a role for autophagy in the pathophysiology of type 1 and type 2 diabetes mellitus. Persistent high concentrations of glucose lead to imbalances in the antioxidant capacity within the cell resulting in oxidative stress-mediated injury in both disorders. An anticipated consequence of impaired autophagy is the accumulation of dysfunctional organelles such as mitochondria within the cell. Mitochondria are the primary site of the production of reactive oxygen species (ROS), and an imbalance in ROS production relative to the cytoprotective action of autophagy may lead to the accumulation of ROS. Impaired mitochondrial function associated with increased ROS levels have been proposed as mechanisms contributing to insulin resistance. In this article we review and interpret the literature that implicates a role for autophagy in the pathophysiology of type 1 and type 2 diabetes mellitus as it applies to β-cell dysfunction, and more broadly to organ systems involved in complications of diabetes including the cardiovascular, renal and nervous systems. Fil: Gonzalez, Claudio D.. Hospital CEMIC; Argentina. Universidad de Buenos Aires; Argentina Fil: Lee, Myung Shik. Samsung Medical Center; Corea del Sur Fil: Marchetti, Piero. Universita Degli Studi Di Pisa; Italia Fil: Pietropaolo, Massimo. University Of Michigan; Estados Unidos Fil: Towns, Roberto. University Of Michigan; Estados Unidos Fil: Vaccaro, Maria Ines. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Ciencias Biológicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay; Argentina Fil: Watada, Hirotaka. Juntendo University. School of Medicine; Japón Fil: Wiley, John W.. University Of Michigan; Estados Unidos |
description |
An emerging body of evidence supports a role for autophagy in the pathophysiology of type 1 and type 2 diabetes mellitus. Persistent high concentrations of glucose lead to imbalances in the antioxidant capacity within the cell resulting in oxidative stress-mediated injury in both disorders. An anticipated consequence of impaired autophagy is the accumulation of dysfunctional organelles such as mitochondria within the cell. Mitochondria are the primary site of the production of reactive oxygen species (ROS), and an imbalance in ROS production relative to the cytoprotective action of autophagy may lead to the accumulation of ROS. Impaired mitochondrial function associated with increased ROS levels have been proposed as mechanisms contributing to insulin resistance. In this article we review and interpret the literature that implicates a role for autophagy in the pathophysiology of type 1 and type 2 diabetes mellitus as it applies to β-cell dysfunction, and more broadly to organ systems involved in complications of diabetes including the cardiovascular, renal and nervous systems. |
publishDate |
2011 |
dc.date.none.fl_str_mv |
2011-01 |
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/11336/13194 Gonzalez, Claudio D.; Lee, Myung Shik; Marchetti, Piero; Pietropaolo, Massimo; Towns, Roberto; et al.; The emerging role of autophagy in the pathophysiology of diabetes mellitus; Landes Bioscience; Autophagy; 7; 1; 1-2011; 2-11 1554-8627 |
url |
http://hdl.handle.net/11336/13194 |
identifier_str_mv |
Gonzalez, Claudio D.; Lee, Myung Shik; Marchetti, Piero; Pietropaolo, Massimo; Towns, Roberto; et al.; The emerging role of autophagy in the pathophysiology of diabetes mellitus; Landes Bioscience; Autophagy; 7; 1; 1-2011; 2-11 1554-8627 |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/doi/10.4161/auto.7.1.13044 info:eu-repo/semantics/altIdentifier/url/http://www.tandfonline.com/doi/abs/10.4161/auto.7.1.13044 |
dc.rights.none.fl_str_mv |
info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
eu_rights_str_mv |
openAccess |
rights_invalid_str_mv |
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/ |
dc.format.none.fl_str_mv |
application/pdf application/pdf |
dc.publisher.none.fl_str_mv |
Landes Bioscience |
publisher.none.fl_str_mv |
Landes Bioscience |
dc.source.none.fl_str_mv |
reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas |
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CONICET Digital (CONICET) |
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CONICET Digital (CONICET) |
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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 |
repository.mail.fl_str_mv |
dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar |
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13.13397 |