Neonatal Apex Resection Triggers Cardiomyocyte Proliferation, Neovascularization and Functional Recovery Despite Local Fibrosis

• Type: Article in International Scientific Journal
• Date: 2018

Authors

Sampaio Pinto, V (Author) Other; Rodrigues, SC (Author) Other; Laundos, TL (Author) Other; Silva, ED (Author) Other; Vasques Novoa, F (Author) FMUP; Silva, AC (Author) Other; Cerqueira, RJ (Author) FMUP; Resende, TP (Author) Other; Pianca, N (Author) Other; Leite-Moreira AF (Author) FMUP; D'Uva, G (Author) Other; Thorsteinsdottir, S (Author) Other; Perpetua Pinto do O (Author) ICBAS; Nascimento, DS (Author) ICBAS

Journal

Title: Stem Cell Reports

Vol. 10

Pages: 860-874

ISSN: 2213-6711

Publisher: Elsevier

Indexing

ISI Web of Knowledge - 24 Citations

Scopus - 26 Citations

Other information

Authenticus ID: P-00N-QZ6

DOI: 10.1016/j.stemcr.2018.01.042

Abstract (EN): 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.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 15