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Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
Published on: June 3, 2018
Regulation of myocardial fibrosis by MicroRNAs
1Medizinische Klinik und Poliklinik I, Universitätsklinikum, Julius-Maximilians-Universität, Würzburg, Germany. bauersachs.johann@mh-hannover.de
Insights
MicroRNAs (miRNAs) regulate cardiac fibrosis, a key factor in heart remodeling after injury. Targeting miRNAs offers a promising new strategy for treating heart fibrosis and failure.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- Fibrosis Research
Background:
- Interstitial and perivascular fibrosis are hallmarks of adverse cardiac remodeling due to stressors like hypertension and myocardial infarction.
- The interaction between cardiac fibroblasts and cardiomyocytes significantly influences hypertrophic responses and cardiac remodeling.
- MicroRNAs (miRNAs) are key regulators of gene expression involved in cardiovascular physiology and pathology.
Purpose of the Study:
- To review current knowledge on how microRNAs (miRNAs) modulate myocardial fibrosis.
- To elucidate miRNA-mediated mechanisms at cellular and subcellular levels in cardiac remodeling.
- To explore the role of miRNAs in the interdependence of cardiac cell types during matrix formation and healing.
Main Methods:
- Literature review of studies on microRNA regulation of myocardial fibrosis.
- Analysis of miRNA mechanisms in cardiac cells and extracellular matrix formation.
- Examination of therapeutic strategies involving miRNA modulation.
Main Results:
- MicroRNAs play a crucial role in regulating myocardial fibrosis and cardiac remodeling.
- Understanding miRNA pathways provides insights into cardiac structural changes induced by various stressors.
- Successful in vivo treatment of cardiac fibrosis using miRNA antagonists (antagomirs) in a murine model was demonstrated.
Conclusions:
- MicroRNAs are essential regulators of myocardial fibrosis and cardiac remodeling.
- Targeting miRNAs presents a novel therapeutic avenue for treating fibrotic heart disease.
- MiRNA-based therapies hold potential for treating fibrotic conditions in the heart and other organs.
Abstract:
Interstitial and perivascular fibrosis is a hallmark of adverse cardiac remodeling in response to stress such as hypertension, valve disease, or myocardial infarction. The cross talk between fibroblasts and cardiomyocytes seems to be a major determinant of the hypertrophic response, and fibroblasts may prove to be essential regulators of cardiac remodeling. The present review summarizes current knowledge on the modulation of myocardial fibrosis by microRNAs (miRNAs), single-stranded molecules consisting of approximately 22 noncoding nucleotides that regulate a variety of target genes involved in cardiovascular (patho)physiology. Dissection of miRNA-mediated mechanisms on myocardial and cellular and subcellular levels will provide insights into the impact of miRNAs for cardiac structural changes induced by different stressors and also expand our understanding of the interdependence of different cell types in the heart with regard to extracellular matrix formation during healing and remodeling after myocardial infarction or in response to pressure overload. The first successful treatment of fibrosis and failure in a murine pressure overload model by application of miRNA antagonists such as antagomirs in vivo raises the hope that manipulating miRNAs may emerge as a novel treatment strategy for fibrotic changes not only in the heart but also in other organs.
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