Autophagy Activation in Zebrafish Heart Regeneration
Author
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Chávez, Myra
Author
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Morales, Rodrigo A.
Author
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López Crisosto, Camila
Author
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Roa, Juan
Author
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Allende Connelly, Miguel
Author
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Lavandero González, Sergio
Admission date
dc.date.accessioned
2020-11-06T15:37:01Z
Available date
dc.date.available
2020-11-06T15:37:01Z
Publication date
dc.date.issued
2020
Cita de ítem
dc.identifier.citation
Scientific Reports (2020) 10:2191
es_ES
Identifier
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10.1038/s41598-020-59106-z
Identifier
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https://repositorio.uchile.cl/handle/2250/177599
Abstract
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Autophagy is an evolutionarily conserved process that plays a key role in the maintenance of overall cellular health. While it has been suggested that autophagy may elicit cardioprotective and pro-survival modulating functions, excessive activation of autophagy can also be detrimental. In this regard, the zebrafish is considered a hallmark model for vertebrate regeneration, since contrary to adult mammals, it is able to faithfully regenerate cardiac tissue. Interestingly, the role that autophagy may play in zebrafish heart regeneration has not been studied yet. In the present work, we hypothesize that, in the context of a well-established injury model of ventricular apex resection, autophagy plays a critical role during cardiac regeneration and its regulation can directly affect the zebrafish regenerative potential. We studied the autophagy events occurring upon injury using electron microscopy, in vivo tracking of autophagy markers, and protein analysis. Additionally, using pharmacological tools, we investigated how rapamycin, an inducer of autophagy, affects regeneration relevant processes. Our results show that a tightly regulated autophagic response is triggered upon injury and during the early stages of the regeneration process. Furthermore, treatment with rapamycin caused an impairment in the cardiac regeneration outcome. These findings are reminiscent of the pathophysiological description of an injured human heart and hence put forward the zebrafish as a model to study the poorly understood double-sword effect that autophagy has in cardiac homeostasis.
es_ES
Patrocinador
dc.description.sponsorship
Agencia Nacional de Investigacion y Desarrollo (ANID), Chile: FONDAP
15130011
15090007
Comision Nacional de Investigacion Cientifica y Tecnologica (CONICYT)
CONICYT FONDECYT
1200490
3160086
3190546
CONICYT PhD Fellowship
21130458