ArticleAmerican journal of physiology. Heart and circulatory physiology2014
Cessation of contraction induces cardiomyocyte remodeling during zebrafish cardiogenesis.
Article in American journal of physiology. Heart and circulatory physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Nonmuscle α-Actinin-4 Couples Sarcomere Function to Cardiac Remodeling.Circulation research · 2026Article
- Cardiac manifestations of human ACTA2 variants recapitulated in a zebrafish model.Journal of human genetics · 2024Article
- Article
- TheFrontiers in physiology · 2023Article
- Myocardial Afterload Is a Key Biomechanical Regulator of Atrioventricular Myocyte Differentiation in Zebrafish.Journal of cardiovascular development and disease · 2022Article
- Article
- Vascularisation of pluripotent stem cell-derived myocardium: biomechanical insights for physiological relevance in cardiac tissue engineering.Pflugers Archiv : European journal of physiology · 2021Review
- Myomesin is part of an integrity pathway that responds to sarcomere damage and disease.PloS one · 2019Article
- Exon- and contraction-dependent functions of titin in sarcomere assembly.Development (Cambridge, England) · 2016Article
- Interplay between cardiac function and heart development.Biochimica et biophysica acta · 2016Review
- Cardiac contraction activates endocardial Notch signaling to modulate chamber maturation in zebrafish.Development (Cambridge, England) · 2015Article
- Cardiac transcriptome and dilated cardiomyopathy genes in zebrafish.Circulation. Cardiovascular genetics · 2015Article
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Authors and funding
4 authors.
Funding
Abstract
Contraction regulates heart development via a complex mechanotransduction process controlled by various mechanical forces. Here, we exploit zebrafish embryos as an in vivo animal model to discern the contribution from different mechanical forces and identify the underlying mechanotransductive signaling pathways of cardiogenesis. We treated 2 days postfertilization zebrafish embryos with Blebbistatin, a myosin II inhibitor, to stop cardiac contraction, which induces a response termed cessation of contraction-induced cardiomyocyte (CM) enlargement (CCE). Accompanying the CCE, lateral fusion of myofibrils was attenuated within CMs. The CCE can be blunted by loss of blood in tail-docked zebrafish but not in cloche mutant fish, suggesting that transmural pressure rather than shear stress is accountable for the chamber enlargement. By screening a panel of small molecule inhibitors, our data suggested essential functions of phosphoinositide 3-kinase signaling and protein synthesis in CCE, which are independent of the sarcomere integrity. In summary, we defined a unique CCE response in genetically tractable zebrafish embryos. A panel of assays was established to verify the contribution from extrinsic forces and interrogate underlying signaling pathways.
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