ArticleCardiovascular research2014
Epicardial calcineurin-NFAT signals through Smad2 to direct coronary smooth muscle cell and arterial wall development.
Article in Cardiovascular research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 16 citations in OpenAlex.
- Novel Insights into the Molecular Mechanisms Governing Embryonic Epicardium Formation.Journal of cardiovascular development and disease · 2023Review
- Calcineurin Is a Universal Regulator of Vessel Function-Focus on Vascular Smooth Muscle Cells.Cells · 2023Review
- Role of calcineurin biosignaling in cell secretion and the possible regulatory mechanisms.Saudi journal of biological sciences · 2021Review
- Rutin inhibits coronary heart disease through ERK1/2 and Akt signaling in a porcine model.Experimental and therapeutic medicine · 2018Article
- Endothelin-1 supports clonal derivation and expansion of cardiovascular progenitors derived from human embryonic stem cells.Nature communications · 2016Article
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11 authors at 3 institutions in 1 country.
Funding
Abstract
aimsCongenital coronary artery anomalies produce serious events that include syncope, arrhythmias, myocardial infarction, or sudden death. Studying the mechanism of coronary development will contribute to the understanding of the disease and help design new diagnostic or therapeutic strategies. Here, we characterized a new calcineurin-NFAT signalling which specifically functions in the epicardium to regulate the development of smooth muscle wall of the coronary arteries. METHODS AND
resultsUsing tissue-specific gene deletion, we found that calcineurin-NFAT signals in the embryonic epicardium to direct coronary smooth muscle cell development. The smooth muscle wall of coronary arteries fails to mature in mice with epicardial deletion of calcineurin B1 (Cnb1), and accordingly these mutant mice develop cardiac dysfunction with reduced exercise capacity. Inhibition of calcineurin at various developmental windows shows that calcineurin-NFAT signals within a narrow time window at embryonic Day 12.5-13.5 to regulate coronary smooth muscle cell development. Within the epicardium, NFAT transcriptionally activates the expression of Smad2, whose gene product is critical for transducing transforming growth factor β (TGFβ)-Alk5 signalling to control coronary development.
conclusionOur findings demonstrate new spatiotemporal and molecular actions of calcineurin-NFAT that dictate coronary arterial wall development and a new mechanism by which calcineurin-NFAT integrates with TGFβ signalling during embryonic development.
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