Key result
Further research into molecules, microRNAs, and matricellular proteins is needed to better understand the mechanisms triggering and maintaining myocardial fibrosis.
This review outlines emerging molecular mechanisms of myocardial fibrosis, highlighting potential new targets for diagnostic and therapeutic interventions.
No fibrosis-specific therapies are supported yet; leaves open molecular targets for future diagnostics and interventions.
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.
No takes yet. Share an insight, caveat, or question.
Heymans et al. (2015) conducted a review in Myocardial fibrosis. Further research into molecules, microRNAs, and matricellular proteins is needed to better understand the mechanisms triggering and maintaining myocardial fibrosis.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: