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
- Institución
- Consejo Nacional de Investigaciones Científicas y Técnicas
- OAI Identificador
- oai:ri.conicet.gov.ar:11336/2257
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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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1842980976072851456 |
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12.993085 |