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
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/80396
Ver los metadatos del registro completo
id |
CONICETDig_47a0e6846175bfcadde08249fe8a99f3 |
---|---|
oai_identifier_str |
oai:ri.conicet.gov.ar:11336/80396 |
network_acronym_str |
CONICETDig |
repository_id_str |
3498 |
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 |
_version_ |
1844614460627484672 |
score |
13.070432 |