Role of Mitochondrial Dysfunction in Hypertension and Obesity

Autores
Lahera Juliá, Vicente; de Las Heras, Natalia; López Farré, Antonio; Manucha, Walter Ariel Fernando; Ferder, León
Año de publicación
2017
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Mitochondria are essential for the maintenance of normal physiological function of tissue cells. Mitochondria are subject to dynamic processes in order to establish a control system related to survival or cell death and adaptation to changes in the metabolic environment of cells. Mitochondrial dynamics includes fusion and fission processes, biogenesis, and mitophagy. Modifications of mitochondrial dynamics in organs involved in energy metabolism such as the pancreas, liver, skeletal muscle, and white adipose tissue could be of relevance for the development of insulin resistance, obesity, and type 2 diabetes. Mitochondrial dynamics and the factors involved in its regulation are also critical for neuronal development, survival, and function. Modifications in mitochondrial dynamics in either agouti-related peptide (AgRP) or pro-opiomelanocortin (POMC), circuits which regulates feeding behavior, are related to changes of food intake, energy balance, and obesity development. Activation of the sympathetic nervous system has been considered as a crucial point in the pathogenesis of hypertension among obese individuals and it also plays a key role in cardiac remodeling. Hypertension-related cardiac hypertrophy is associated with changes in metabolic substrate utilization, dysfunction of the electron transport chain, and ATP synthesis. Alterations in both mitochondrial dynamics and ROS production have been associated with endothelial dysfunction, development of hypertension, and cardiac hypertrophy. Finally, it might be postulated that alterations of mitochondrial dynamics in white adipose tissue could contribute to the development and maintenance of hypertension in obesity situations through leptin overproduction. Leptin, together with insulin, will induce activation of sympathetic nervous system with consequences at renal, vascular, and cardiac levels, driving to sodium retention, hypertension, and left ventricular hypertrophy. Moreover, both leptin and insulin will induce mitochondrial alterations into arcuate nucleus leading to signals driving to increased food intake and reduced energy expenditure. This, in turn would perpetuate white adipose tissue excess and its well-known metabolic and cardiovascular consequences.
Fil: Lahera Juliá, Vicente. Universidad Complutense de Madrid. Facultad de Medicina. Departamento de Fisiología; España
Fil: de Las Heras, Natalia. Universidad Complutense de Madrid. Facultad de Medicina; España
Fil: López Farré, Antonio. Universidad Complutense de Madrid. Facultad de Medicina. Departamento de Fisiología; España
Fil: Manucha, Walter Ariel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; Argentina
Fil: Ferder, León. Universidad de Miami; Estados Unidos
Materia
Hypertension
Mitochondrial Dynamics
Mitochondrial Dysfunction
Obesity
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/49726
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/49726
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Role of Mitochondrial Dysfunction in Hypertension and ObesityLahera Juliá, Vicentede Las Heras, NataliaLópez Farré, AntonioManucha, Walter Ariel FernandoFerder, LeónHypertensionMitochondrial DynamicsMitochondrial DysfunctionObesityhttps://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3Mitochondria are essential for the maintenance of normal physiological function of tissue cells. Mitochondria are subject to dynamic processes in order to establish a control system related to survival or cell death and adaptation to changes in the metabolic environment of cells. Mitochondrial dynamics includes fusion and fission processes, biogenesis, and mitophagy. Modifications of mitochondrial dynamics in organs involved in energy metabolism such as the pancreas, liver, skeletal muscle, and white adipose tissue could be of relevance for the development of insulin resistance, obesity, and type 2 diabetes. Mitochondrial dynamics and the factors involved in its regulation are also critical for neuronal development, survival, and function. Modifications in mitochondrial dynamics in either agouti-related peptide (AgRP) or pro-opiomelanocortin (POMC), circuits which regulates feeding behavior, are related to changes of food intake, energy balance, and obesity development. Activation of the sympathetic nervous system has been considered as a crucial point in the pathogenesis of hypertension among obese individuals and it also plays a key role in cardiac remodeling. Hypertension-related cardiac hypertrophy is associated with changes in metabolic substrate utilization, dysfunction of the electron transport chain, and ATP synthesis. Alterations in both mitochondrial dynamics and ROS production have been associated with endothelial dysfunction, development of hypertension, and cardiac hypertrophy. Finally, it might be postulated that alterations of mitochondrial dynamics in white adipose tissue could contribute to the development and maintenance of hypertension in obesity situations through leptin overproduction. Leptin, together with insulin, will induce activation of sympathetic nervous system with consequences at renal, vascular, and cardiac levels, driving to sodium retention, hypertension, and left ventricular hypertrophy. Moreover, both leptin and insulin will induce mitochondrial alterations into arcuate nucleus leading to signals driving to increased food intake and reduced energy expenditure. This, in turn would perpetuate white adipose tissue excess and its well-known metabolic and cardiovascular consequences.Fil: Lahera Juliá, Vicente. Universidad Complutense de Madrid. Facultad de Medicina. Departamento de Fisiología; EspañaFil: de Las Heras, Natalia. Universidad Complutense de Madrid. Facultad de Medicina; EspañaFil: López Farré, Antonio. Universidad Complutense de Madrid. Facultad de Medicina. Departamento de Fisiología; EspañaFil: Manucha, Walter Ariel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; ArgentinaFil: Ferder, León. Universidad de Miami; Estados UnidosCurrent Medicine Group2017-02info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/49726Lahera Juliá, Vicente; de Las Heras, Natalia; López Farré, Antonio; Manucha, Walter Ariel Fernando; Ferder, León; Role of Mitochondrial Dysfunction in Hypertension and Obesity; Current Medicine Group; Current Hypertension Reports; 19; 11; 2-2017; 1-91522-64171534-3111CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/doi/10.1007/s11906-017-0710-9info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007%2Fs11906-017-0710-9info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-10T13:02:38Zoai:ri.conicet.gov.ar:11336/49726instacron: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:34982025-09-10 13:02:39.093CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Role of Mitochondrial Dysfunction in Hypertension and Obesity
title Role of Mitochondrial Dysfunction in Hypertension and Obesity
spellingShingle Role of Mitochondrial Dysfunction in Hypertension and Obesity
Lahera Juliá, Vicente
Hypertension
Mitochondrial Dynamics
Mitochondrial Dysfunction
Obesity
title_short Role of Mitochondrial Dysfunction in Hypertension and Obesity
title_full Role of Mitochondrial Dysfunction in Hypertension and Obesity
title_fullStr Role of Mitochondrial Dysfunction in Hypertension and Obesity
title_full_unstemmed Role of Mitochondrial Dysfunction in Hypertension and Obesity
title_sort Role of Mitochondrial Dysfunction in Hypertension and Obesity
dc.creator.none.fl_str_mv Lahera Juliá, Vicente
de Las Heras, Natalia
López Farré, Antonio
Manucha, Walter Ariel Fernando
Ferder, León
author Lahera Juliá, Vicente
author_facet Lahera Juliá, Vicente
de Las Heras, Natalia
López Farré, Antonio
Manucha, Walter Ariel Fernando
Ferder, León
author_role author
author2 de Las Heras, Natalia
López Farré, Antonio
Manucha, Walter Ariel Fernando
Ferder, León
author2_role author
author
author
author
dc.subject.none.fl_str_mv Hypertension
Mitochondrial Dynamics
Mitochondrial Dysfunction
Obesity
topic Hypertension
Mitochondrial Dynamics
Mitochondrial Dysfunction
Obesity
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.3
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Mitochondria are essential for the maintenance of normal physiological function of tissue cells. Mitochondria are subject to dynamic processes in order to establish a control system related to survival or cell death and adaptation to changes in the metabolic environment of cells. Mitochondrial dynamics includes fusion and fission processes, biogenesis, and mitophagy. Modifications of mitochondrial dynamics in organs involved in energy metabolism such as the pancreas, liver, skeletal muscle, and white adipose tissue could be of relevance for the development of insulin resistance, obesity, and type 2 diabetes. Mitochondrial dynamics and the factors involved in its regulation are also critical for neuronal development, survival, and function. Modifications in mitochondrial dynamics in either agouti-related peptide (AgRP) or pro-opiomelanocortin (POMC), circuits which regulates feeding behavior, are related to changes of food intake, energy balance, and obesity development. Activation of the sympathetic nervous system has been considered as a crucial point in the pathogenesis of hypertension among obese individuals and it also plays a key role in cardiac remodeling. Hypertension-related cardiac hypertrophy is associated with changes in metabolic substrate utilization, dysfunction of the electron transport chain, and ATP synthesis. Alterations in both mitochondrial dynamics and ROS production have been associated with endothelial dysfunction, development of hypertension, and cardiac hypertrophy. Finally, it might be postulated that alterations of mitochondrial dynamics in white adipose tissue could contribute to the development and maintenance of hypertension in obesity situations through leptin overproduction. Leptin, together with insulin, will induce activation of sympathetic nervous system with consequences at renal, vascular, and cardiac levels, driving to sodium retention, hypertension, and left ventricular hypertrophy. Moreover, both leptin and insulin will induce mitochondrial alterations into arcuate nucleus leading to signals driving to increased food intake and reduced energy expenditure. This, in turn would perpetuate white adipose tissue excess and its well-known metabolic and cardiovascular consequences.
Fil: Lahera Juliá, Vicente. Universidad Complutense de Madrid. Facultad de Medicina. Departamento de Fisiología; España
Fil: de Las Heras, Natalia. Universidad Complutense de Madrid. Facultad de Medicina; España
Fil: López Farré, Antonio. Universidad Complutense de Madrid. Facultad de Medicina. Departamento de Fisiología; España
Fil: Manucha, Walter Ariel Fernando. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Ciencias Médicas; Argentina
Fil: Ferder, León. Universidad de Miami; Estados Unidos
description Mitochondria are essential for the maintenance of normal physiological function of tissue cells. Mitochondria are subject to dynamic processes in order to establish a control system related to survival or cell death and adaptation to changes in the metabolic environment of cells. Mitochondrial dynamics includes fusion and fission processes, biogenesis, and mitophagy. Modifications of mitochondrial dynamics in organs involved in energy metabolism such as the pancreas, liver, skeletal muscle, and white adipose tissue could be of relevance for the development of insulin resistance, obesity, and type 2 diabetes. Mitochondrial dynamics and the factors involved in its regulation are also critical for neuronal development, survival, and function. Modifications in mitochondrial dynamics in either agouti-related peptide (AgRP) or pro-opiomelanocortin (POMC), circuits which regulates feeding behavior, are related to changes of food intake, energy balance, and obesity development. Activation of the sympathetic nervous system has been considered as a crucial point in the pathogenesis of hypertension among obese individuals and it also plays a key role in cardiac remodeling. Hypertension-related cardiac hypertrophy is associated with changes in metabolic substrate utilization, dysfunction of the electron transport chain, and ATP synthesis. Alterations in both mitochondrial dynamics and ROS production have been associated with endothelial dysfunction, development of hypertension, and cardiac hypertrophy. Finally, it might be postulated that alterations of mitochondrial dynamics in white adipose tissue could contribute to the development and maintenance of hypertension in obesity situations through leptin overproduction. Leptin, together with insulin, will induce activation of sympathetic nervous system with consequences at renal, vascular, and cardiac levels, driving to sodium retention, hypertension, and left ventricular hypertrophy. Moreover, both leptin and insulin will induce mitochondrial alterations into arcuate nucleus leading to signals driving to increased food intake and reduced energy expenditure. This, in turn would perpetuate white adipose tissue excess and its well-known metabolic and cardiovascular consequences.
publishDate 2017
dc.date.none.fl_str_mv 2017-02
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/11336/49726
Lahera Juliá, Vicente; de Las Heras, Natalia; López Farré, Antonio; Manucha, Walter Ariel Fernando; Ferder, León; Role of Mitochondrial Dysfunction in Hypertension and Obesity; Current Medicine Group; Current Hypertension Reports; 19; 11; 2-2017; 1-9
1522-6417
1534-3111
CONICET Digital
CONICET
url http://hdl.handle.net/11336/49726
identifier_str_mv Lahera Juliá, Vicente; de Las Heras, Natalia; López Farré, Antonio; Manucha, Walter Ariel Fernando; Ferder, León; Role of Mitochondrial Dysfunction in Hypertension and Obesity; Current Medicine Group; Current Hypertension Reports; 19; 11; 2-2017; 1-9
1522-6417
1534-3111
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1007/s11906-017-0710-9
info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007%2Fs11906-017-0710-9
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 Current Medicine Group
publisher.none.fl_str_mv Current Medicine Group
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv 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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score 12.993085

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