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ESC Heart Fail. 2018 Feb;5(1):139-148. doi: 10.1002/ehf2.12218. Epub 2017 Oct 7.

Rationale of the FIBROTARGETS study designed to identify novel biomarkers of myocardial fibrosis.

Author information

1
Centre d'Investigation Clinique 1433 Module Plurithématique, INSERM U1116, Université de Lorraine, CHRU de Nancy, F-CRIN INI-CRCT, Hopitaux de Brabois, Institut Lorrain du Coeur et des Vaisseaux Louis Mathieu, 4 rue du Morvan, 54500, Vandœuvre-lès-Nancy, France.
2
Department of Physiology and Cardiothoracic Surgery, Cardiovascular Research and Development Unit, Faculty of Medicine, University of Porto, Porto, Portugal.
3
Centre de Recherche des Cordeliers, Inserm U1138, Université Pierre et Marie Curie, Paris, France.
4
Institute of Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Hanover, Germany.
5
National Heart and Lung Institute, Imperial College London, London, UK.
6
Cardiology Division, Stony Brook University, Stony Brook, NY, USA.
7
Program of Cardiovascular Diseases, Center for Applied Medical Research, University of Navarra, Pamplona, Spain.
8
Department of Cardiology and Cardiac Surgery, University of Navarra Clinic, Pamplona, Spain.
9
CIBERCV, Institute of Health Carlos III, Madrid, Spain.
10
Center for Heart Failure Research, Cardiovascular Research Institute Maastricht (CARIM), University Hospital Maastricht, Maastricht, The Netherlands.
11
University College Dublin, Dublin, Ireland.
12
Department of Cardiology, Medical University of Vienna, Vienna, Austria.
13
Firalis S.A.S., Huningue, France.

Abstract

AIMS:

Myocardial fibrosis alters the cardiac architecture favouring the development of cardiac dysfunction, including arrhythmias and heart failure. Reducing myocardial fibrosis may improve outcomes through the targeted diagnosis and treatment of emerging fibrotic pathways. The European-Commission-funded 'FIBROTARGETS' is a multinational academic and industrial consortium with the main aims of (i) characterizing novel key mechanistic pathways involved in the metabolism of fibrillary collagen that may serve as biotargets, (ii) evaluating the potential anti-fibrotic properties of novel or repurposed molecules interfering with the newly identified biotargets, and (iii) characterizing bioprofiles based on distinct mechanistic phenotypes involving the aforementioned biotargets. These pathways will be explored by performing a systematic and collaborative search for mechanisms and targets of myocardial fibrosis. These mechanisms will then be translated into individualized diagnostic tools and specific therapeutic pharmacological options for heart failure.

METHODS AND RESULTS:

The FIBROTARGETS consortium has merged data from 12 patient cohorts in a common database available to individual consortium partners. The database consists of >12 000 patients with a large spectrum of cardiovascular clinical phenotypes. It integrates community-based population cohorts, cardiovascular risk cohorts, and heart failure cohorts.

CONCLUSIONS:

The FIBROTARGETS biomarker programme is aimed at exploring fibrotic pathways allowing the bioprofiling of patients into specific 'fibrotic' phenotypes and identifying new therapeutic targets that will potentially enable the development of novel and tailored anti-fibrotic therapies for heart failure.

KEYWORDS:

Fibrotic bioprofiles; Heart failure; Myocardial fibrosis

PMID:
28988439
PMCID:
PMC5793978
DOI:
10.1002/ehf2.12218
[Indexed for MEDLINE]
Free PMC Article

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