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Título
Telomerase Is Essential for Zebrafish Heart Regeneration
Autor(es)
Bednarek, Dorota CNIC | Gonzalez-Rosa, Juan Manuel CNIC | Guzman-Martinez, Gabriela CNIC | Gutierrez-Gutierrez, Oscar CNIC | Aguado, Tania CNIC | Sanchez-Ferrer, Carlota CNIC | Marques, Ines Joao CNIC | Galardi-Castilla, Maria CNIC | de Diego, Irene CNIC | Gomez, Manuel J CNIC | Cortes, Alfonso | Zapata, Agustin | Jimenez-Borreguero, Luis J. CNIC | Mercader, Nadia CNIC | Flores, Ignacio CNIC
Fecha de publicación
2015
Cita
Cell Rep. 2015; 12(10):1691-703
Idioma
Inglés
Tipo de documento
journal article
Resumen
After myocardial infarction in humans, lost cardiomyocytes are replaced
by an irreversible fibrotic scar. In contrast, zebrafish hearts
efficiently regenerate after injury. Complete regeneration of the
zebrafish heart is driven by the strong proliferation response of its
cardiomyocytes to injury. Here we show that, after cardiac injury in
zebrafish, telomerase becomes hyperactivated, and telomeres elongate
transiently, preceding a peak of cardiomyocyte proliferation and full
organ recovery. Using a telomerase-mutant zebrafish model, we found that
telomerase loss drastically decreases cardiomyocyte proliferation and
fibrotic tissue regression after cryoinjury and that cardiac function
does not recover. The impaired cardiomyocyte proliferation response is
accompanied by the absence of cardiomyocytes with long telomeres and an
increased proportion of cardiomyocytes showing DNA damage and senescence
characteristics. These findings demonstrate the importance of telomerase
function in heart regeneration and highlight the potential of telomerase
therapy as a means of stimulating cell proliferation upon myocardial
infarction.
Palabras clave
CARDIOMYOCYTE PROLIFERATION | MYOCARDIAL-INFARCTION | INJURY | CRYOINJURY | CAPACITY | MODEL | HEMATOPOIESIS | ACTIVATION | EXPRESSION | FAILURE
Versión en línea
DOI
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