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

Stephane Heymans, Arantxa Gonzalez, Anne Pizard, Anna P. Papageorgiou, Natalia Lopez-Andres, Frederic Jaisser, Thomas Thum, Faiez Zannad, Javier Diez*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review


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.
Original languageEnglish
Pages (from-to)764-771
JournalEuropean journal of heart failure
Issue number8
Publication statusPublished - Aug 2015


  • Heart failure
  • Interstitial fibrosis
  • Therapeutic targets


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