ArticleDevelopment (Cambridge, England)2025
Voltage-gated calcium channels generate blastema Ca2+ fluxes restraining zebrafish fin regenerative outgrowth.
Article in Development (Cambridge, England), 2025. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Injury-induced electrochemical coupling triggers organ growth.Science advances · 2026Article
Corrections and comments
- Update of
Authors and funding
6 authors.
Funding
Abstract
Adult zebrafish fins regenerate to their original size regardless of damage extent, providing a tractable organ size control model. Gain-of-function of voltage-gated K+ channels in fibroblast-lineage blastema cells or inhibition of the Ca2+-dependent phosphatase calcineurin causes dramatic fin regenerative overgrowth. However, Ca2+ fluxes and their potential origins from dynamic membrane voltages have not been directly linked to fin size restoration. We used fibroblast-lineage GCaMP imaging of regenerating fins to identify widespread Ca2+ transients in distal blastema cells. Membrane depolarization of isolated fin fibroblasts triggered voltage-gated Ca2+ channel-dependent Ca2+ spikes. Single cell transcriptomics identified cacna1c (L-type channel), cacna1ba (N-type) and cacna1g (T-type) as candidate mediators of fibroblast-lineage Ca2+ signaling. Small molecule inhibition revealed that L- and/or N-type channels act during regenerative outgrowth to restore fins to their original scale. Strikingly, cacna1g homozygous mutant zebrafish regenerated extraordinarily long fins due to prolonged outgrowth. GCaMP imaging showed Cacna1g enables Ca2+ dynamics in the distal blastema. We conclude that 'bioelectricity' for fin size control reflects voltage-modulated Ca²+ fluxes in fibroblast-lineage blastemal cells that decelerate outgrowth at a rate tuned to restore the original scale of the fin.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.