University of Oulu

Laura E. Vainio, Zoltán Szabó, Ruizhu Lin, Johanna Ulvila, Raisa Yrjölä, Tarja Alakoski, Jarkko Piuhola, Walter J. Koch, Heikki Ruskoaho, Shaun D. Fouse, Todd W. Seeley, Erhe Gao, Pierre Signore, Kenneth E. Lipson, Johanna Magga, Risto Kerkelä, Connective Tissue Growth Factor Inhibition Enhances Cardiac Repair and Limits Fibrosis After Myocardial Infarction, JACC: Basic to Translational Science, Volume 4, Issue 1, 2019, Pages 83-94, ISSN 2452-302X,

Connective tissue growth factor inhibition enhances cardiac repair and limits fibrosis after myocardial infarction

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Author: Vainio, Laura E.1,2; Szabó, Zoltán1,2; Lin, Ruizhu1;
Organizations: 1Research Unit of Biomedicine, Department of Pharmacology and Toxicology, University of Oulu, Oulu, Finland
2Biocenter Oulu, University of Oulu, Oulu, Finland
3Division of Cardiology, Department of Internal Medicine, Oulu University Hospital and University of Oulu, Oulu, Finland
4Center for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania
5Division of Pharmacology and Pharmacotherapy, Faculty of Pharmacy, University of Helsinki, Helsinki, Finland
6FibroGen, Inc., San Francisco, California
7Medical Research Center Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland
Format: article
Version: published version
Access: open
Online Access: PDF Full Text (PDF, 2.2 MB)
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Language: English
Published: Elsevier, 2019
Publish Date: 2020-04-09


Myocardial infarction (MI)−induced cardiac fibrosis attenuates cardiac contractile function, and predisposes to arrhythmias and sudden cardiac death. Expression of connective tissue growth factor (CTGF) is elevated in affected organs in virtually every fibrotic disorder and in the diseased human myocardium. Mice were subjected to treatment with a CTGF monoclonal antibody (mAb) during infarct repair, post-MI left ventricular (LV) remodeling, or acute ischemia−reperfusion injury. CTGF mAb therapy during infarct repair improved survival and reduced LV dysfunction, and reduced post-MI LV hypertrophy and fibrosis. Mechanistically, CTGF mAb therapy induced expression of cardiac developmental and/or repair genes and attenuated expression of inflammatory and/or fibrotic genes.

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Series: JACC. Basic to translational science
ISSN: 2452-302X
ISSN-E: 2452-302X
ISSN-L: 2452-302X
Volume: 4
Issue: 1
Pages: 83 - 94
DOI: 10.1016/j.jacbts.2018.10.007
Type of Publication: A1 Journal article – refereed
Field of Science: 3121 General medicine, internal medicine and other clinical medicine
Funding: Drs. Vainio, Magga, and Kerkelä were supported by the Finnish Foundation for Cardiovascular Research. Dr. Vainio was supported by the Finnish Medical Foundation. Dr. Magga was supported by grant 268505 from the Academy of Finland. Dr. Kerkelä was supported by grants 131020 and 297094 from the Academy of Finland, by the Sigrid Juselius Foundation, and by the Jane and Aatos Erkko Foundation. Drs. Fouse, Seeley, Signore, and Lipson hold stock in FibroGen. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
Academy of Finland Grant Number: 268505
Detailed Information: 268505 (Academy of Finland Funding decision)
131020 (Academy of Finland Funding decision)
297094 (Academy of Finland Funding decision)
Copyright information: © 2019 The Authors. Published by Elsevier on behalf of the American College of Cardiology Foundation. This is an open access article under the CC BY-NC-ND license (