Methods for studying primary cilia in heart tissue after ischemia-reperfusion injury

Catalina Kretschmar, María Paz Hernández-Cáceres, Montserrat Reyes, Daniel Peña-Oyarzún, Camila García-Navarrete, Rodrigo Troncoso, Francisco Díaz-Castro, Mauricio Budini, Eugenia Morselli, Jaime A. Riquelme, Joseph A. Hill, Sergio Lavandero*, Alfredo Criollo

*Corresponding author for this work

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review


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.

Original languageEnglish
Title of host publicationCilia
Subtitle of host publicationFrom Mechanisms to Disease - Part B
EditorsJosé Manuel Bravo-San Pedro, Lorenzo Galluzzi
PublisherAcademic Press Inc.
Number of pages17
ISBN (Print)9780443185885
StatePublished - 2023

Publication series

NameMethods in Cell Biology
ISSN (Print)0091-679X

Bibliographical note

Publisher Copyright:
© 2023 Elsevier Inc.

ASJC Scopus subject areas

  • Cell Biology


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