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Iron accumulation drives fibrosis, senescence and the senescence-associated secretory phenotype
dc.contributor.author | Maus, Mate | |
dc.contributor.author | López-Polo, Vanessa | |
dc.contributor.author | Mateo, Lidia | |
dc.contributor.author | Lafarga, Miguel | |
dc.contributor.author | Aguilera, Mònica | |
dc.contributor.author | De Lama, Eugenia | |
dc.contributor.author | Meyer, Kathleen | |
dc.contributor.author | Sola, Anna | |
dc.contributor.author | Lopez-Martinez, Cecilia | |
dc.contributor.author | López-Alonso, Ines | |
dc.contributor.author | Guasch-Piqueras, Marc | |
dc.contributor.author | Hernandez-Gonzalez, Fernanda | |
dc.contributor.author | Chaib, Selim | |
dc.contributor.author | Rovira, Miguel | |
dc.contributor.author | Sanchez, Mayka | |
dc.contributor.author | Faner, Rosa | |
dc.contributor.author | Agusti, Alvar | |
dc.contributor.author | Diéguez-Hurtado, Rodrigo | |
dc.contributor.author | Ortega, Sagrario | |
dc.contributor.author | Manonelles, Anna | |
dc.contributor.author | Engelhardt, Stefan | |
dc.contributor.author | Monteiro, Freddy | |
dc.contributor.author | Stephan-Otto Attolini, Camille | |
dc.contributor.author | Prats, Neus | |
dc.contributor.author | Albaiceta, Guillermo | |
dc.contributor.author | Cruzado, Josep M. | |
dc.contributor.author | Serrano, Manuel | |
dc.date.accessioned | 2024-01-24T14:52:39Z | |
dc.date.available | 2024-01-24T14:52:39Z | |
dc.date.issued | 2023 | |
dc.identifier.citation | Maus, Mate; López-Polo, Vanessa; Mateo, Lidia [et al.]. Iron accumulation drives fibrosis, senescence and the senescence-associated secretory phenotype. Nature Metabolism, 2023, 5, p. 2111-2130. Disponible en: <https://www.nature.com/articles/s42255-023-00928-2>. Fecha de acceso: 24 ene. 2024. DOI: 10.1038/s42255-023-00928-2 | ca |
dc.identifier.issn | 2522-5812 | ca |
dc.identifier.uri | http://hdl.handle.net/20.500.12328/3961 | |
dc.description.abstract | Fibrogenesis is part of a normal protective response to tissue injury that can become irreversible and progressive, leading to fatal diseases. Senescent cells are a main driver of fibrotic diseases through their secretome, known as senescence-associated secretory phenotype (SASP). Here, we report that cellular senescence, and multiple types of fibrotic diseases in mice and humans are characterized by the accumulation of iron. We show that vascular and hemolytic injuries are efficient in triggering iron accumulation, which in turn can cause senescence and promote fibrosis. Notably, we find that senescent cells persistently accumulate iron, even when the surge of extracellular iron has subdued. Indeed, under normal conditions of extracellular iron, cells exposed to different types of senescence-inducing insults accumulate abundant ferritin-bound iron, mostly within lysosomes, and present high levels of labile iron, which fuels the generation of reactive oxygen species and the SASP. Finally, we demonstrate that detection of iron by magnetic resonance imaging might allow non-invasive assessment of fibrotic burden in the kidneys of mice and in patients with renal fibrosis. Our findings suggest that iron accumulation plays a central role in senescence and fibrosis, even when the initiating events may be independent of iron, and identify iron metabolism as a potential therapeutic target for senescence-associated diseases. | ca |
dc.format.extent | 40 | ca |
dc.language.iso | eng | ca |
dc.publisher | Springer Nature | ca |
dc.relation.ispartof | Nature Metabolism | ca |
dc.relation.ispartofseries | 5 | |
dc.rights | This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. | ca |
dc.subject.other | Envelliment | ca |
dc.subject.other | Ferro | ca |
dc.subject.other | Mecanismes de la malaltia | ca |
dc.subject.other | Metabolisme | ca |
dc.subject.other | Senescència | ca |
dc.subject.other | Envejecimiento | ca |
dc.subject.other | Hierro | ca |
dc.subject.other | Mecanismos de enfermedad | ca |
dc.subject.other | Metabolismo | ca |
dc.subject.other | Senectud | ca |
dc.subject.other | Ageing | ca |
dc.subject.other | Iron | ca |
dc.subject.other | Mechanisms of disease | ca |
dc.subject.other | Metabolism | ca |
dc.subject.other | Senescence | ca |
dc.title | Iron accumulation drives fibrosis, senescence and the senescence-associated secretory phenotype | ca |
dc.type | info:eu-repo/semantics/article | ca |
dc.description.version | info:eu-repo/semantics/publishedVersion | ca |
dc.rights.accessLevel | info:eu-repo/semantics/openAccess | |
dc.embargo.terms | cap | ca |
dc.subject.udc | 61 | ca |
dc.identifier.doi | https://dx.doi.org/10.1038/s42255-023-00928-2 | ca |
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