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00925njm 22002777a 4500 dc Bednarek, Dorota author Gonzalez-Rosa, Juan Manuel author Guzman-Martinez, Gabriela author Gutierrez-Gutierrez, Oscar author Aguado, Tania author Sanchez-Ferrer, Carlota author Marques, Ines Joao author Galardi-Castilla, Maria author de Diego, Irene author Gomez, Manuel J author Cortes, Alfonso author Zapata, Agustin author Jimenez-Borreguero, Luis J. author Mercader, Nadia author Flores, Ignacio author 2015 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. Cell Rep. 2015; 12(10):1691-703 10.1016/j.celrep.2015.07.064 2211-1247 Cell Reports 26321646 http://hdl.handle.net/20.500.12105/5391 CARDIOMYOCYTE PROLIFERATION MYOCARDIAL-INFARCTION INJURY CRYOINJURY CAPACITY MODEL HEMATOPOIESIS ACTIVATION EXPRESSION FAILURE Telomerase Is Essential for Zebrafish Heart Regeneration