Hypertension and Insulin Resistance: Implications of Mitochondrial Dysfunction

Autores
Manucha, Walter Ariel Fernando; Ritchie, Bob; Ferder, León
Año de publicación
2014
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Mitochondria are the primary generators of cellular reactive oxygen species (ROS); their pathophysiological roles in hypertension and insulin resistance are but imperfectly understood. Mitochondrial dysfunction has been linked to the etiologies of many complex diseases, but many other factors, including the upregulation of the renin-angiotensin system (RAS) and vitamin D deficiency, have also been implicated in hypertension pathogenesis. Hypertension resulting from the disruption of the RAS contributes to the risk of cardiovascular disease. Likewise, experimental and clinical evidence indicate that RAS stimulation and low vitamin D levels are inversely related and represent risk factors associated with the pathogenesis of hypertension. Furthermore, RAS activation induces insulin resistance, resulting in increases in ROS levels. High levels of ROS are harmful to cells, having the potential to trigger both mitochondrial-mediated apoptosis and the degradation of the mitochondrial DNA. Diabetes risk is also associated with high levels of oxidative stress; taking vitamin D, however, may reduce that risk. The finding that mitochondria possess both a functional RAS and vitamin D receptors is the starting point for improving our understanding of the interaction of mitochondria and chronic disease states, which understanding should lead to decreases in the chronic disease burden attributable to hypertension, diabetes, or both.
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: Ritchie, Bob. Ponce School Of Medicine; Puerto Rico
Fil: Ferder, León. Ponce School Of Medicine; Puerto Rico
Materia
Angiotensin Ii
Heat-Shock Protein 70
Hypertension
Insulin Resistance
Mitochondrial Dysfunction
Vitamin D
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:11336/80396

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network_name_str CONICET Digital (CONICET)
spelling Hypertension and Insulin Resistance: Implications of Mitochondrial DysfunctionManucha, Walter Ariel FernandoRitchie, BobFerder, LeónAngiotensin IiHeat-Shock Protein 70HypertensionInsulin ResistanceMitochondrial DysfunctionVitamin Dhttps://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3Mitochondria are the primary generators of cellular reactive oxygen species (ROS); their pathophysiological roles in hypertension and insulin resistance are but imperfectly understood. Mitochondrial dysfunction has been linked to the etiologies of many complex diseases, but many other factors, including the upregulation of the renin-angiotensin system (RAS) and vitamin D deficiency, have also been implicated in hypertension pathogenesis. Hypertension resulting from the disruption of the RAS contributes to the risk of cardiovascular disease. Likewise, experimental and clinical evidence indicate that RAS stimulation and low vitamin D levels are inversely related and represent risk factors associated with the pathogenesis of hypertension. Furthermore, RAS activation induces insulin resistance, resulting in increases in ROS levels. High levels of ROS are harmful to cells, having the potential to trigger both mitochondrial-mediated apoptosis and the degradation of the mitochondrial DNA. Diabetes risk is also associated with high levels of oxidative stress; taking vitamin D, however, may reduce that risk. The finding that mitochondria possess both a functional RAS and vitamin D receptors is the starting point for improving our understanding of the interaction of mitochondria and chronic disease states, which understanding should lead to decreases in the chronic disease burden attributable to hypertension, diabetes, or both.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; ArgentinaFil: Ritchie, Bob. Ponce School Of Medicine; Puerto RicoFil: Ferder, León. Ponce School Of Medicine; Puerto RicoSpringer2014-11info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/80396Manucha, Walter Ariel Fernando; Ritchie, Bob; Ferder, León; Hypertension and Insulin Resistance: Implications of Mitochondrial Dysfunction; Springer; Current Hypertension Reports; 17; 1; 11-2014; 1-71522-6417CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://link.springer.com/article/10.1007%2Fs11906-014-0504-2info:eu-repo/semantics/altIdentifier/doi/10.1007/s11906-014-0504-2info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:42:43Zoai:ri.conicet.gov.ar:11336/80396instacron: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:34982025-09-29 10:42:43.466CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Hypertension and Insulin Resistance: Implications of Mitochondrial Dysfunction
title Hypertension and Insulin Resistance: Implications of Mitochondrial Dysfunction
spellingShingle Hypertension and Insulin Resistance: Implications of Mitochondrial Dysfunction
Manucha, Walter Ariel Fernando
Angiotensin Ii
Heat-Shock Protein 70
Hypertension
Insulin Resistance
Mitochondrial Dysfunction
Vitamin D
title_short Hypertension and Insulin Resistance: Implications of Mitochondrial Dysfunction
title_full Hypertension and Insulin Resistance: Implications of Mitochondrial Dysfunction
title_fullStr Hypertension and Insulin Resistance: Implications of Mitochondrial Dysfunction
title_full_unstemmed Hypertension and Insulin Resistance: Implications of Mitochondrial Dysfunction
title_sort Hypertension and Insulin Resistance: Implications of Mitochondrial Dysfunction
dc.creator.none.fl_str_mv Manucha, Walter Ariel Fernando
Ritchie, Bob
Ferder, León
author Manucha, Walter Ariel Fernando
author_facet Manucha, Walter Ariel Fernando
Ritchie, Bob
Ferder, León
author_role author
author2 Ritchie, Bob
Ferder, León
author2_role author
author
dc.subject.none.fl_str_mv Angiotensin Ii
Heat-Shock Protein 70
Hypertension
Insulin Resistance
Mitochondrial Dysfunction
Vitamin D
topic Angiotensin Ii
Heat-Shock Protein 70
Hypertension
Insulin Resistance
Mitochondrial Dysfunction
Vitamin D
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 the primary generators of cellular reactive oxygen species (ROS); their pathophysiological roles in hypertension and insulin resistance are but imperfectly understood. Mitochondrial dysfunction has been linked to the etiologies of many complex diseases, but many other factors, including the upregulation of the renin-angiotensin system (RAS) and vitamin D deficiency, have also been implicated in hypertension pathogenesis. Hypertension resulting from the disruption of the RAS contributes to the risk of cardiovascular disease. Likewise, experimental and clinical evidence indicate that RAS stimulation and low vitamin D levels are inversely related and represent risk factors associated with the pathogenesis of hypertension. Furthermore, RAS activation induces insulin resistance, resulting in increases in ROS levels. High levels of ROS are harmful to cells, having the potential to trigger both mitochondrial-mediated apoptosis and the degradation of the mitochondrial DNA. Diabetes risk is also associated with high levels of oxidative stress; taking vitamin D, however, may reduce that risk. The finding that mitochondria possess both a functional RAS and vitamin D receptors is the starting point for improving our understanding of the interaction of mitochondria and chronic disease states, which understanding should lead to decreases in the chronic disease burden attributable to hypertension, diabetes, or both.
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: Ritchie, Bob. Ponce School Of Medicine; Puerto Rico
Fil: Ferder, León. Ponce School Of Medicine; Puerto Rico
description Mitochondria are the primary generators of cellular reactive oxygen species (ROS); their pathophysiological roles in hypertension and insulin resistance are but imperfectly understood. Mitochondrial dysfunction has been linked to the etiologies of many complex diseases, but many other factors, including the upregulation of the renin-angiotensin system (RAS) and vitamin D deficiency, have also been implicated in hypertension pathogenesis. Hypertension resulting from the disruption of the RAS contributes to the risk of cardiovascular disease. Likewise, experimental and clinical evidence indicate that RAS stimulation and low vitamin D levels are inversely related and represent risk factors associated with the pathogenesis of hypertension. Furthermore, RAS activation induces insulin resistance, resulting in increases in ROS levels. High levels of ROS are harmful to cells, having the potential to trigger both mitochondrial-mediated apoptosis and the degradation of the mitochondrial DNA. Diabetes risk is also associated with high levels of oxidative stress; taking vitamin D, however, may reduce that risk. The finding that mitochondria possess both a functional RAS and vitamin D receptors is the starting point for improving our understanding of the interaction of mitochondria and chronic disease states, which understanding should lead to decreases in the chronic disease burden attributable to hypertension, diabetes, or both.
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/11336/80396
Manucha, Walter Ariel Fernando; Ritchie, Bob; Ferder, León; Hypertension and Insulin Resistance: Implications of Mitochondrial Dysfunction; Springer; Current Hypertension Reports; 17; 1; 11-2014; 1-7
1522-6417
CONICET Digital
CONICET
url http://hdl.handle.net/11336/80396
identifier_str_mv Manucha, Walter Ariel Fernando; Ritchie, Bob; Ferder, León; Hypertension and Insulin Resistance: Implications of Mitochondrial Dysfunction; Springer; Current Hypertension Reports; 17; 1; 11-2014; 1-7
1522-6417
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/http://link.springer.com/article/10.1007%2Fs11906-014-0504-2
info:eu-repo/semantics/altIdentifier/doi/10.1007/s11906-014-0504-2
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
application/pdf
dc.publisher.none.fl_str_mv Springer
publisher.none.fl_str_mv Springer
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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