دورية أكاديمية
Neonatal Apex Resection Triggers Cardiomyocyte Proliferation, Neovascularization and Functional Recovery Despite Local Fibrosis
| العنوان: | Neonatal Apex Resection Triggers Cardiomyocyte Proliferation, Neovascularization and Functional Recovery Despite Local Fibrosis |
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| المؤلفون: | Sampaio-Pinto, V, Rodrigues, SC, Laundos, TL, Silva, ED, Vasques-Nóvoa, F, Silva, AC, Cerqueira, R, Resende, TP, Pianca, N, Leite-Moreira, A, D'Uva, G, Thorsteinsdóttir, S, Pinto-do-Ó, P, Nascimento, DS |
| المساهمون: | Instituto de Investigação e Inovação em Saúde |
| بيانات النشر: | Cell Press |
| سنة النشر: | 2018 |
| المجموعة: | Repositório Aberto da Universidade do Porto |
| مصطلحات موضوعية: | Animals, Newborn, Cell Proliferation / physiology, Fibrosis / physiopathology, Heart / physiology, Heart Injuries / physiopathology, Heart Ventricles / physiopathology, Mice, Inbred C57BL, Myocardium / pathology, Myocytes, Cardiac / physiology, Neovascularization, Pathologic / physiopathology, Recovery of Function / physiology, Regeneration / physiology |
| الوصف: | 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. ; The authors acknowledge the support of i3S scientific platforms (animal facility, ALM, HEMS, BSU, b.IMAGE, CCGEN, TraCy). The authors are thankful to current and past members of Pinto-do-Ó laboratory for the critical discussion. This work was financed by Norte Portugal Regional Operational Programme (NORTE 2020), under the PORTUGAL 2020 Partnership Agreement, through the European Regional Development Fund (ERDF) ( NORTE-01-0145-FEDER-000012 ); by European Structural and Investment Funds (ESIF), under Lisbon Portugal Regional Operational Programme and National Funds through FCT (Fundação para a Ciência e Tecnologia [ Foundation for Science and Technology ] [ POCI-01-0145-FEDER-016385 ]); by INFARMED – Autoridade Nacional do Medicamento e Produtos de Saúde , I.P. ( FIS-FIS-2015-01_CCV_20150630-157 ); and by FCT/ Ministério da Ciência, Tecnologia e Inovação in the framework of the project “Institute for Research and Innovation in Health Sciences” ( POCI-01-0145- FEDER-007274 ) and individual ... |
| نوع الوثيقة: | article in journal/newspaper |
| وصف الملف: | application/pdf |
| اللغة: | English |
| تدمد: | 2213-6711 |
| العلاقة: | info:eu-repo/grantAgreement/FCT/SFRH/SFRH%2FBD%2F88780%2F2012/PT; info:eu-repo/grantAgreement/FCT/SFRH/SFRH%2FBPD%2F80588%2F2011/PT; Stem Cell Reports, vol.10(3), p. 860-874; https://www.sciencedirect.com/science/article/pii/S2213671118300687?via%3DihubTest; https://hdl.handle.net/10216/127423Test |
| DOI: | 10.1016/j.stemcr.2018.01.042 |
| الإتاحة: | https://doi.org/10.1016/j.stemcr.2018.01.042Test https://hdl.handle.net/10216/127423Test |
| حقوق: | info:eu-repo/semantics/openAccess |
| رقم الانضمام: | edsbas.ACFCA0B2 |
| قاعدة البيانات: | BASE |
Full Text Finder | تدمد: | 22136711 |
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| DOI: | 10.1016/j.stemcr.2018.01.042 |