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Searching for new mechanisms of myocardial fibrosis with diagnostic and/or therapeutic potential
Author(s) -
Heymans Stephane,
González Arantxa,
Pizard Anne,
Papageorgiou Anna P.,
LópezAndrés Natalia,
Jaisser Frédéric,
Thum Thomas,
Zannad Faiez,
Díez Javier
Publication year - 2015
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1002/ejhf.312
Subject(s) - lysyl oxidase , medicine , fibrosis , matricellular protein , myocardial fibrosis , myofibroblast , galectin 3 , heart failure , cardiac fibrosis , cardiology , bioinformatics , microbiology and biotechnology , extracellular matrix , biology
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.