Journal
STEM CELL REPORTS
Volume 10, Issue 3, Pages 860-874Publisher
CELL PRESS
DOI: 10.1016/j.stemcr.2018.01.042
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Funding
- Norte Portugal Regional Operational Programme (NORTE)
- PORTUGAL Partnership Agreement
- European Regional Development Fund (ERDF) [NORTE-01-0145-FEDER-000012]
- European Structural and Investment Funds (ESIF)
- Lisbon Portugal Regional Operational Programme
- National Funds through FCT (Fundacao para a Ciencia e Tecnologia [Foundation for Science and Technology] [POCI-01-0145-FEDER-016385]
- INFARMED - Autoridade Nacional do Medicamento e Produtos de Saude, I.P. [FIS-FIS-2015-01_CCV_20150630-157]
- FCT/Ministerio da Ciencia, Tecnologia e Inovacao [POCI-01-0145-FEDER-007274, SFRH/BD/111799/2015, PD/BD/127997/2016, SFRH/BD/88780/2012, SFRH/BPD/80588/2011]
- Fundação para a Ciência e a Tecnologia [SFRH/BD/88780/2012, PD/BD/127997/2016, SFRH/BD/111799/2015] Funding Source: FCT
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So far, opposing outcomes have been reported following neonatal apex resection in mice, questioning the validity of this injury model to investigate regenerative mechanisms. We performed a systematic evaluation, up to 180 days after surgery, of the pathophysiological events activated upon apex resection. In response to cardiac injury, we observed increased cardiomyocyte proliferation in remote and apex regions, neovascularization, and local fibrosis. In adulthood, resected hearts remain consistently shorter and display permanent fibrotic tissue deposition in the center of the resection plane, indicating limited apex regrowth. However, thickening of the left ventricle wall, explained by an upsurge in cardiomyocyte proliferation during the initial response to injury, compensated cardiomyocyte loss and supported normal systolic function. Thus, apex resection triggers both regenerative and reparative mechanisms, endorsing this injury model for studies aimed at promoting cardiomyocyte proliferation and/or downplaying fibrosis.
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