Searching for new mechanisms of myocardial fibrosis with diagnostic and/or therapeutic potential: Corrigendum to 'Searching for new mechanisms of myocardial fibrosis with diagnostic and/or therapeutic potential'[Eur J Heart Fail 2015; 17:764-771].

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.
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Submitted on : Wednesday, April 4, 2018 - 3:53:23 PM
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Stephane Heymans, Arantxa González, Anne Pizard, Anna Papageorgiou, Natalia López-Andrés, et al.. Searching for new mechanisms of myocardial fibrosis with diagnostic and/or therapeutic potential: Corrigendum to 'Searching for new mechanisms of myocardial fibrosis with diagnostic and/or therapeutic potential'[Eur J Heart Fail 2015; 17:764-771].. European Journal of Heart Failure, Oxford University Press (OUP), 2015, 17 (8), pp.764 - 771. ⟨10.1002/ejhf.312⟩. ⟨hal-01758592⟩

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