ArticleGenesis (New York, N.Y. : 2000)2026
Pvr and Pvf2 Are Essential for Valve Cell Differentiation in the Larval Drosophila Heart.
Article in Genesis (New York, N.Y. : 2000), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Pvr and Pvf2 Are Essential for Valve Cell Differentiation in the Larval Drosophila Heart.Genesis (New York, N.Y. : 2000) · 2026Article
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Authors and funding
4 authors.
Funding
Abstract
The directionality of blood flow is regulated by heart valves, among other things. While the heart valves in vertebrates are multicellular and complex, the valve in the Drosophila heart consists of exactly two highly specialized cells. They arise during early larval development from two cardiomyocytes, those that form the boundary between the aorta and the posterior ventricle. Here, we show that the conserved PDGF signaling pathway is involved in the determination of heart valve cells. RNAi-mediated knockdown of the Pvr receptor and one of its ligands, Pvf2, leads to an inhibition of valve cell differentiation. In contrast, the simultaneous expression of the Pvr and Pvf2 in the entire heart tube leads to the formation of additional heart valve cells in ectopic positions. A single expression of the receptor or the ligand does not lead to heart valve formation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.