ArticleDevelopment (Cambridge, England)2024
Mechanical forces remodel the cardiac extracellular matrix during zebrafish development.
Article in Development (Cambridge, England), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Restoration of structural organization in engineered cardiac microtissues is promoted by cardiomyocyte beating.Communications biology · 2026Article
- Transformative biomechanics and mechanobiology breakthroughs shaping the future of health and medicine.Innovation (Cambridge (Mass.)) · 2026Review
- Integrated NEK7-inflammasome and platelet transcriptomic signature generates mechanistic hypotheses in heart failure.PloS one · 2026Article
- morphoHeart: A quantitative tool for integrated 3D morphometric analyses of heart and ECM during embryonic development.PLoS biology · 2025Article
- Distinct mechanisms regulate ventricular and atrial chamber wall formation.Nature communications · 2024Article
- The heart is a resident tissue for hematopoietic stem and progenitor cells in zebrafish.Nature communications · 2024Article
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Authors and funding
7 authors.
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Abstract
The cardiac extracellular matrix (cECM) is fundamental for organ morphogenesis and maturation, during which time it undergoes remodeling, yet little is known about whether mechanical forces generated by the heartbeat regulate this remodeling process. Using zebrafish as a model and focusing on stages when cardiac valves and trabeculae form, we found that altering cardiac contraction impairs cECM remodeling. Longitudinal volumetric quantifications in wild-type animals revealed region-specific dynamics: cECM volume decreases in the atrium but not in the ventricle or atrioventricular canal. Reducing cardiac contraction resulted in opposite effects on the ventricular and atrial ECM, whereas increasing the heart rate affected the ventricular ECM but had no effect on the atrial ECM, together indicating that mechanical forces regulate the cECM in a chamber-specific manner. Among the ECM remodelers highly expressed during cardiac morphogenesis, we found one that was upregulated in non-contractile hearts, namely tissue inhibitor of matrix metalloproteinase 2 (timp2). Loss- and gain-of-function analyses of timp2 revealed its crucial role in cECM remodeling. Altogether, our results indicate that mechanical forces control cECM remodeling in part through timp2 downregulation.
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