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dc.contributor.author
Martini, Nancy
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dc.contributor.author
Streckwall, Lucas
dc.contributor.author
McCarthy, Antonio Desmond
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dc.date.available
2024-01-11T14:13:24Z
dc.date.issued
2023-09
dc.identifier.citation
Martini, Nancy; Streckwall, Lucas; McCarthy, Antonio Desmond; Osteoporosis and vascular calcifications; BioScientifica; Endocrine Connections; 12; 11; 9-2023; 1-13
dc.identifier.issn
2049-3614
dc.identifier.uri
http://hdl.handle.net/11336/223391
dc.description.abstract
In post-menopausal women, aged individuals, and patients with diabetes mellitus or chronic renal disease, bone mineral density (BMD) decreases while the vasculature accumulates arterial calcifications (ACs). AC can be found in the tunica intima and/or in the tunica media. Prospective studies have shown that patients with initially low BMD and/or the presence of fragility fractures have at follow-up a significantly increased risk for coronary and cerebrovascular events and for overall cardiovascular mortality. Similarly, patients presenting with abdominal aorta calcifications (an easily quantifiable marker of vascular pathology) show a significant decrease in the BMD (and an increase in the fragility) of bones irrigated by branches of the abdominal aorta, such as the hip and lumbar spine. AC induction is an ectopic tissue biomineralization process promoted by osteogenic transdifferentiation of vascular smooth muscle cells as well as by local and systemic secreted factors. In many cases, the same regulatory molecules modulate bone metabolism but in reverse. Investigation of animal and in vitro models has identified several potential mechanisms for this reciprocal bone–vascular regulation, such as vitamin K and D sufficiency, advanced glycation end-products–RAGE interaction, osteoprotegerin/RANKL/RANK, Fetuin A, oestrogen deficiency and phytooestrogen supplementation, microbiota and its relation to diet, among others. Complete elucidation of these potential mechanisms, as well as their clinical validation via controlled studies, will provide a basis for pharmacological intervention that could simultaneously promote bone and vascular health.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
BioScientifica
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
ARTERIAL CALCIFICATIONS
dc.subject
BONE FRACTURES
dc.subject
CARDIOVASCULAR DISEASE
dc.subject
OSTEOGENIC TRANSDIFFERENTIATION
dc.subject
OSTEOPOROSIS
dc.subject
VASCULAR SMOOTH MUSCLE CELLS
dc.subject.classification
Bioquímica y Biología Molecular
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dc.subject.classification
Ciencias Biológicas
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dc.subject.classification
CIENCIAS NATURALES Y EXACTAS
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dc.title
Osteoporosis and vascular calcifications
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2024-01-10T13:51:24Z
dc.journal.volume
12
dc.journal.number
11
dc.journal.pagination
1-13
dc.journal.pais
Reino Unido
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dc.journal.ciudad
Bristol
dc.description.fil
Fil: Martini, Nancy. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata; Argentina. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Ciencias Biológicas. Laboratorio de Investigación en Osteospatías y Metabolismo Mineral; Argentina
dc.description.fil
Fil: Streckwall, Lucas. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Ciencias Biológicas. Laboratorio de Investigación en Osteospatías y Metabolismo Mineral; Argentina
dc.description.fil
Fil: McCarthy, Antonio Desmond. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Departamento de Ciencias Biológicas. Laboratorio de Investigación en Osteospatías y Metabolismo Mineral; Argentina
dc.journal.title
Endocrine Connections
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://ec.bioscientifica.com/view/journals/ec/aop/ec-23-0305/ec-23-0305.xml
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1530/EC-23-0305
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