Methods for studying primary cilia in heart tissue after ischemia-reperfusion injury
Author
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Kretschmar, Catalina
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Hernández Cáceres, María Paz
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Reyes Rojas, Montserrat
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Peña Oyarzún, Daniel
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García Navarrete, Camila
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Troncoso Cotal, Rodrigo Hernán
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Díaz Castro, Francisco
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Budini Budini, Mauricio Fernando
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Morselli, Eugenia
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Riquelme Meléndez, Jaime Andrés
Author
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Hill, Joseph A.
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Lavandero González, Sergio
Author
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Criollo Céspedes, Alfredo
Admission date
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2024-03-11T20:32:35Z
Available date
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2024-03-11T20:32:35Z
Publication date
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2023
Cita de ítem
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En: Bravo-San Pedro, José Manuel ; Galluzzi, Lorenzo. Cilia: From Mechanisms to Disease - Part B. Elsevier, 2023. pp. 85-101 ISBN 9780443185885
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Identifier
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10.1016/bs.mcb.2022.12.013
Identifier
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https://repositorio.uchile.cl/handle/2250/197335
Abstract
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Cardiovascular diseases are the leading cause of death and disability worldwide. After heart injury triggered by myocardial ischemia or myocardial infarction, extensive zones of tissue are damaged and some of the tissue dies by necrosis and/or apoptosis. The loss of contractile mass activates a series of biochemical mechanisms that allow, through cardiac remodeling, the replacement of the dysfunctional heart tissue by fibrotic material. Our previous studies have shown that primary cilia, non-motile antenna-like structures at the cell surface required for the activation of specific signaling pathways, are present in cardiac fibroblasts and required for cardiac fibrosis induced by ischemia/reperfusion (I/R) in mice. I/R-induced myocardial fibrosis promotes the enrichment of ciliated cardiac fibroblasts where the myocardial injury occurs. Given discussions about the existence of cilia in specific cardiac cell types, as well as the functional relevance of studying cilia-dependent signaling in cardiac fibrosis after I/R, here we describe our methods to evaluate the presence and roles of primary cilia in cardiac fibrosis after I/R in mice.
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Lenguage
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en
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Publisher
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Elsevier
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Serie
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Methods in Cell Biology;Vol. 176
Type of license
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Attribution-NonCommercial-NoDerivs 3.0 United States