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dc.contributor.author | Latorre, Marcos![]() |
es_ES |
dc.contributor.author | Spronck, Bart![]() |
es_ES |
dc.contributor.author | Humphrey, Jay D.![]() |
es_ES |
dc.date.accessioned | 2023-01-31T19:00:17Z | |
dc.date.available | 2023-01-31T19:00:17Z | |
dc.date.issued | 2021-01-27 | es_ES |
dc.identifier.issn | 1364-5021 | es_ES |
dc.identifier.uri | http://hdl.handle.net/10251/191545 | |
dc.description.abstract | [EN] Arteries are exposed to relentless pulsatile haemodynamic loads, but via mechanical homeostasis they tend to maintain near optimal structure, properties and function over long periods in maturity in health. Numerous insults can compromise such homeostatic tendencies, however, resulting in maladaptations or disease. Chronic inflammation can be counted among the detrimental insults experienced by arteries, yet inflammation can also play important homeostatic roles. In this paper, we present a new theoretical model of complementary mechanobiological and immunobiological control of vascular geometry and composition, and thus properties and function. We motivate and illustrate the model using data for aortic remodelling in a common mouse model of induced hypertension. Predictions match the available data well, noting a need for increased data for further parameter refinement. The overall approach and conclusions are general, however, and help to unify two previously disparate literatures, thus leading to deeper insight into the separate and overlapping roles of mechanobiology and immunobiology in vascular health and disease. | es_ES |
dc.description.sponsorship | This work was supported, in part, by grants from the US National Institutes of Health (grant nos. R01 HL105297, P01 HL134605, R01 HL146723) | es_ES |
dc.language | Inglés | es_ES |
dc.publisher | The Royal Society | es_ES |
dc.relation.ispartof | Proceedings of the Royal Society A: Mathematical, Physical and Engineering Sciences | es_ES |
dc.rights | Reconocimiento (by) | es_ES |
dc.subject | Hypertension | es_ES |
dc.subject | Mechanotransduction | es_ES |
dc.subject | Inflammation | es_ES |
dc.subject | Homeostasis | es_ES |
dc.subject | Artery | es_ES |
dc.title | Complementary roles of mechanotransduction and inflammation in vascular homeostasis | es_ES |
dc.type | Artículo | es_ES |
dc.identifier.doi | 10.1098/rspa.2020.0622 | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/NIH//R01 HL105297//Mechanisms Underlying the Progression of Arterial Stiffness in Hypertension/ | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/NIH//P01 HL134605 //Endothelial Mechanotransduction in Thoracic Aneurysm Formation and Progression/ | es_ES |
dc.relation.projectID | info:eu-repo/grantAgreement/NIH//R01 HL146723//Smooth Muscle Cell Proliferation and Degradative Phenotype in Thoracic Aorta Aneurysm and Dissection/ | es_ES |
dc.rights.accessRights | Abierto | es_ES |
dc.description.bibliographicCitation | Latorre, M.; Spronck, B.; Humphrey, JD. (2021). Complementary roles of mechanotransduction and inflammation in vascular homeostasis. Proceedings of the Royal Society A: Mathematical, Physical and Engineering Sciences. 477(2245):1-22. https://doi.org/10.1098/rspa.2020.0622 | es_ES |
dc.description.accrualMethod | S | es_ES |
dc.relation.publisherversion | https://doi.org/10.1098/rspa.2020.0622 | es_ES |
dc.description.upvformatpinicio | 1 | es_ES |
dc.description.upvformatpfin | 22 | es_ES |
dc.type.version | info:eu-repo/semantics/publishedVersion | es_ES |
dc.description.volume | 477 | es_ES |
dc.description.issue | 2245 | es_ES |
dc.identifier.pmid | 33642928 | es_ES |
dc.identifier.pmcid | PMC7897647 | es_ES |
dc.relation.pasarela | S\472455 | es_ES |
dc.contributor.funder | National Institutes of Health, EEUU | es_ES |
dc.subject.ods | 03.- Garantizar una vida saludable y promover el bienestar para todos y todas en todas las edades | es_ES |