The world pandemic of vitamin D deficit culd possibly be explained by cellular inflammatory response activity induced by the renin angiotensin system

Autores
Ferder, Marcelo; Inserra, Pablo Ignacio Felipe; Manucha, Walter Ariel Fernando; Ferder, León
Año de publicación
2013
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
This review attempts to show that there may be a relationship between inflammatory processes induced by chronic overstimulation of the renin-angiotensin system (RAS) and the worldwide deficiency of vitamin D (VitD) and that both disorders are probably associated with environmental factors. Low VitD levels represent a risk factor for several apparently different diseases, such as infectious, autoimmune, neurodegenerative, and cardiovascular diseases, as well as diabetes, osteoporosis, and cancer. Moreover, VitD insufficiency seems to predispose to hypertension, metabolic syndrome, left ventricular hypertrophy, heart failure, and chronic vascular inflammation. On the other hand, inappropriate stimulation of the RAS has also been associated with the pathogenesis of hypertension, heart attack, stroke, and hypertrophy of the left ventricle and vascular smooth muscle cells. Because VitD receptors (VDRs) and RAS receptors are almost distributed in the same tissues, a possible link between VitD and the RAS is even more plausible. Furthermore, from an evolutionary point of view, both systems were developed simultaneously, actively participating in the regulation of inflammatory and immunological mechanisms. Changes in RAS activity and activation of the VDR seem to be inversely related; thus any changes in one of these systems would have a completely opposite effect on the other, making it possible to speculate that the two systems could have a feedback relationship. In fact, the pandemic of VitD deficiency could be the other face of increased RAS activity, which probably causes lower activity or lower levels of VitD. Finally, from a therapeutic point of view, the combination of RAS blockade and VDR stimulation appears to be more effective than either RAS blockade or VDR stimulation individually.
Fil: Ferder, Marcelo. Universidad de Buenos Aires. Facultad de Medicina; Argentina;
Fil: Inserra, Pablo Ignacio Felipe. Universidad Austral. Facultad de Cs.biomedicas; Argentina;
Fil: Manucha, Walter Ariel Fernando. Universidad Nacional de Cuyo; Argentina; Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - CONICET - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina;
Fil: Ferder, León. Ponce School of Medicine and Health Sciences; Puerto Rico;
Materia
Vitamin D
Hypertension
Ras
Pandemia
Oxidative Stress
Mitochondria
Cardiovascular Disease
Angiotensin Receptor Blocker
Vitamin D Receptor
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:11336/2257

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network_name_str CONICET Digital (CONICET)
spelling The world pandemic of vitamin D deficit culd possibly be explained by cellular inflammatory response activity induced by the renin angiotensin systemFerder, MarceloInserra, Pablo Ignacio FelipeManucha, Walter Ariel FernandoFerder, LeónVitamin DHypertensionRasPandemiaOxidative StressMitochondriaCardiovascular DiseaseAngiotensin Receptor BlockerVitamin D Receptorhttps://purl.org/becyt/ford/3.3https://purl.org/becyt/ford/3This review attempts to show that there may be a relationship between inflammatory processes induced by chronic overstimulation of the renin-angiotensin system (RAS) and the worldwide deficiency of vitamin D (VitD) and that both disorders are probably associated with environmental factors. Low VitD levels represent a risk factor for several apparently different diseases, such as infectious, autoimmune, neurodegenerative, and cardiovascular diseases, as well as diabetes, osteoporosis, and cancer. Moreover, VitD insufficiency seems to predispose to hypertension, metabolic syndrome, left ventricular hypertrophy, heart failure, and chronic vascular inflammation. On the other hand, inappropriate stimulation of the RAS has also been associated with the pathogenesis of hypertension, heart attack, stroke, and hypertrophy of the left ventricle and vascular smooth muscle cells. Because VitD receptors (VDRs) and RAS receptors are almost distributed in the same tissues, a possible link between VitD and the RAS is even more plausible. Furthermore, from an evolutionary point of view, both systems were developed simultaneously, actively participating in the regulation of inflammatory and immunological mechanisms. Changes in RAS activity and activation of the VDR seem to be inversely related; thus any changes in one of these systems would have a completely opposite effect on the other, making it possible to speculate that the two systems could have a feedback relationship. In fact, the pandemic of VitD deficiency could be the other face of increased RAS activity, which probably causes lower activity or lower levels of VitD. Finally, from a therapeutic point of view, the combination of RAS blockade and VDR stimulation appears to be more effective than either RAS blockade or VDR stimulation individually.Fil: Ferder, Marcelo. Universidad de Buenos Aires. Facultad de Medicina; Argentina;Fil: Inserra, Pablo Ignacio Felipe. Universidad Austral. Facultad de Cs.biomedicas; Argentina;Fil: Manucha, Walter Ariel Fernando. Universidad Nacional de Cuyo; Argentina; Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - CONICET - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina;Fil: Ferder, León. Ponce School of Medicine and Health Sciences; Puerto Rico;American Physiological Society2013-01-30info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/2257Ferder, Marcelo; Inserra, Pablo Ignacio Felipe; Manucha, Walter Ariel Fernando; Ferder, León; The world pandemic of vitamin D deficit culd possibly be explained by cellular inflammatory response activity induced by the renin angiotensin system; American Physiological Society; American Journal Of Physiology-cell Physiology; 304; 30-1-2013; C1027-C10390363-6143enginfo:eu-repo/semantics/altIdentifier/doi/10.1152/ajpcell.00403.2011info:eu-repo/semantics/altIdentifier/url/http://ajpcell.physiology.org/content/304/11/C1027info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-10T13:17:51Zoai:ri.conicet.gov.ar:11336/2257instacron: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 13:17:51.628CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv The world pandemic of vitamin D deficit culd possibly be explained by cellular inflammatory response activity induced by the renin angiotensin system
title The world pandemic of vitamin D deficit culd possibly be explained by cellular inflammatory response activity induced by the renin angiotensin system
spellingShingle The world pandemic of vitamin D deficit culd possibly be explained by cellular inflammatory response activity induced by the renin angiotensin system
Ferder, Marcelo
Vitamin D
Hypertension
Ras
Pandemia
Oxidative Stress
Mitochondria
Cardiovascular Disease
Angiotensin Receptor Blocker
Vitamin D Receptor
title_short The world pandemic of vitamin D deficit culd possibly be explained by cellular inflammatory response activity induced by the renin angiotensin system
title_full The world pandemic of vitamin D deficit culd possibly be explained by cellular inflammatory response activity induced by the renin angiotensin system
title_fullStr The world pandemic of vitamin D deficit culd possibly be explained by cellular inflammatory response activity induced by the renin angiotensin system
title_full_unstemmed The world pandemic of vitamin D deficit culd possibly be explained by cellular inflammatory response activity induced by the renin angiotensin system
title_sort The world pandemic of vitamin D deficit culd possibly be explained by cellular inflammatory response activity induced by the renin angiotensin system
dc.creator.none.fl_str_mv Ferder, Marcelo
Inserra, Pablo Ignacio Felipe
Manucha, Walter Ariel Fernando
Ferder, León
author Ferder, Marcelo
author_facet Ferder, Marcelo
Inserra, Pablo Ignacio Felipe
Manucha, Walter Ariel Fernando
Ferder, León
author_role author
author2 Inserra, Pablo Ignacio Felipe
Manucha, Walter Ariel Fernando
Ferder, León
author2_role author
author
author
dc.subject.none.fl_str_mv Vitamin D
Hypertension
Ras
Pandemia
Oxidative Stress
Mitochondria
Cardiovascular Disease
Angiotensin Receptor Blocker
Vitamin D Receptor
topic Vitamin D
Hypertension
Ras
Pandemia
Oxidative Stress
Mitochondria
Cardiovascular Disease
Angiotensin Receptor Blocker
Vitamin D Receptor
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.3
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv This review attempts to show that there may be a relationship between inflammatory processes induced by chronic overstimulation of the renin-angiotensin system (RAS) and the worldwide deficiency of vitamin D (VitD) and that both disorders are probably associated with environmental factors. Low VitD levels represent a risk factor for several apparently different diseases, such as infectious, autoimmune, neurodegenerative, and cardiovascular diseases, as well as diabetes, osteoporosis, and cancer. Moreover, VitD insufficiency seems to predispose to hypertension, metabolic syndrome, left ventricular hypertrophy, heart failure, and chronic vascular inflammation. On the other hand, inappropriate stimulation of the RAS has also been associated with the pathogenesis of hypertension, heart attack, stroke, and hypertrophy of the left ventricle and vascular smooth muscle cells. Because VitD receptors (VDRs) and RAS receptors are almost distributed in the same tissues, a possible link between VitD and the RAS is even more plausible. Furthermore, from an evolutionary point of view, both systems were developed simultaneously, actively participating in the regulation of inflammatory and immunological mechanisms. Changes in RAS activity and activation of the VDR seem to be inversely related; thus any changes in one of these systems would have a completely opposite effect on the other, making it possible to speculate that the two systems could have a feedback relationship. In fact, the pandemic of VitD deficiency could be the other face of increased RAS activity, which probably causes lower activity or lower levels of VitD. Finally, from a therapeutic point of view, the combination of RAS blockade and VDR stimulation appears to be more effective than either RAS blockade or VDR stimulation individually.
Fil: Ferder, Marcelo. Universidad de Buenos Aires. Facultad de Medicina; Argentina;
Fil: Inserra, Pablo Ignacio Felipe. Universidad Austral. Facultad de Cs.biomedicas; Argentina;
Fil: Manucha, Walter Ariel Fernando. Universidad Nacional de Cuyo; Argentina; Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico - CONICET - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina;
Fil: Ferder, León. Ponce School of Medicine and Health Sciences; Puerto Rico;
description This review attempts to show that there may be a relationship between inflammatory processes induced by chronic overstimulation of the renin-angiotensin system (RAS) and the worldwide deficiency of vitamin D (VitD) and that both disorders are probably associated with environmental factors. Low VitD levels represent a risk factor for several apparently different diseases, such as infectious, autoimmune, neurodegenerative, and cardiovascular diseases, as well as diabetes, osteoporosis, and cancer. Moreover, VitD insufficiency seems to predispose to hypertension, metabolic syndrome, left ventricular hypertrophy, heart failure, and chronic vascular inflammation. On the other hand, inappropriate stimulation of the RAS has also been associated with the pathogenesis of hypertension, heart attack, stroke, and hypertrophy of the left ventricle and vascular smooth muscle cells. Because VitD receptors (VDRs) and RAS receptors are almost distributed in the same tissues, a possible link between VitD and the RAS is even more plausible. Furthermore, from an evolutionary point of view, both systems were developed simultaneously, actively participating in the regulation of inflammatory and immunological mechanisms. Changes in RAS activity and activation of the VDR seem to be inversely related; thus any changes in one of these systems would have a completely opposite effect on the other, making it possible to speculate that the two systems could have a feedback relationship. In fact, the pandemic of VitD deficiency could be the other face of increased RAS activity, which probably causes lower activity or lower levels of VitD. Finally, from a therapeutic point of view, the combination of RAS blockade and VDR stimulation appears to be more effective than either RAS blockade or VDR stimulation individually.
publishDate 2013
dc.date.none.fl_str_mv 2013-01-30
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/11336/2257
Ferder, Marcelo; Inserra, Pablo Ignacio Felipe; Manucha, Walter Ariel Fernando; Ferder, León; The world pandemic of vitamin D deficit culd possibly be explained by cellular inflammatory response activity induced by the renin angiotensin system; American Physiological Society; American Journal Of Physiology-cell Physiology; 304; 30-1-2013; C1027-C1039
0363-6143
url http://hdl.handle.net/11336/2257
identifier_str_mv Ferder, Marcelo; Inserra, Pablo Ignacio Felipe; Manucha, Walter Ariel Fernando; Ferder, León; The world pandemic of vitamin D deficit culd possibly be explained by cellular inflammatory response activity induced by the renin angiotensin system; American Physiological Society; American Journal Of Physiology-cell Physiology; 304; 30-1-2013; C1027-C1039
0363-6143
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1152/ajpcell.00403.2011
info:eu-repo/semantics/altIdentifier/url/http://ajpcell.physiology.org/content/304/11/C1027
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 American Physiological Society
publisher.none.fl_str_mv American Physiological Society
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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