Searching for new mechanisms of myocardial fibrosis with diagnostic and/or therapeutic potential.

Abstract

Myocardial fibrosis is the result of excessive fibrillar collagen synthesis and deposition without reciprocally balanced degradation. It causes cardiac dysfunction, arrhythmias, and ischaemia, and thereby determines the clinical course and outcome of cardiac patients even when adequately treated. Therefore, further research is needed to identify and better understand the factors that trigger and maintain the myocardial fibrotic response against different injuries in a variety of cardiac diseases. Here, we will focus on the following major areas of research: molecules that stimulate the differentiation of fibroblasts into myofibroblasts and subsequently alter collagen turnover (e.g. cardiotrophin-1, galectin-3, NADPH oxidases, and neutrophil gelatinase-associated lipocalin), microRNA-induced alterations of collagen gene expression, and matricellular protein- and lysyl oxidase-mediated alterations of collagen cross-linking and deposition.

• Authors: Stephane Heymans, Arantxa González, Anne Pizard, Anna P Papageorgiou, Natalia López-Andrés, Frédéric Jaisser, Thomas Thum, Faiez Zannad, Javier Díez
• Journal: European journal of heart failure (Eur J Heart Fail) Vol. 17 Issue 8 Pg. 764-71 (Aug 2015) ISSN: 1879-0844 [Electronic] England
• PMID: 26126780 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
• Copyright: © 2015 The Authors. European Journal of Heart Failure © 2015 European Society of Cardiology.

Chemical References

• CCN Intercellular Signaling Proteins
• Cytokines
• Galectin 3
• MicroRNAs
• Collagen
• cardiotrophin 1
• Protein-Lysine 6-Oxidase
• NADPH Oxidases

Topics

• Animals
• CCN Intercellular Signaling Proteins (metabolism)
• Collagen (genetics, metabolism)
• Cytokines (metabolism)
• Fibroblasts (pathology)
• Fibrosis (pathology)
• Galectin 3 (physiology)
• Gene Expression
• Heart Failure (pathology)
• Humans
• MicroRNAs (analysis)
• Myocardium (pathology)
• NADPH Oxidases (physiology)
• Protein-Lysine 6-Oxidase (physiology)