Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
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.
2 · The registry
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.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
17 authors.
Janita MintchevaLaboratory for Quantitative Developmental Biology, Berlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.
Tzu-Lun TsengDepartment of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.ORCID 0000-0003-1319-0141
Pinelopi GoumenakiDepartment of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Anika NeuschulzLaboratory for Quantitative Developmental Biology, Berlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.ORCID 0000-0001-6163-3344
Anis SenoussiLaboratory for Quantitative Developmental Biology, Berlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.ORCID 0000-0002-7066-8917
Sara LelekLaboratory for Electrochemical Signaling in Development and Disease, Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.
Khai Lone LimInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.ORCID 0000-0003-0295-330X
Zhitao MingDepartment of Genetics, Development and Cell Biology, Iowa State University, Ames, IA, USA.
Ronny SchäferLaboratory for Quantitative Developmental Biology, Berlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.
Alisa HnatiukCenter for Regenerative Therapies TU Dresden, Dresden, Germany.
Nikolay NinovCenter for Regenerative Therapies TU Dresden, Dresden, Germany.ORCID 0000-0003-3286-6100
Arica BeisawMechanisms of Cardiac Regeneration and Repair Lab, Institute of Experimental Cardiology, Heidelberg University, Heidelberg, Germany.ORCID 0000-0002-6658-6978
Maura McGrailDepartment of Genetics, Development and Cell Biology, Iowa State University, Ames, IA, USA.ORCID 0000-0001-9308-6189
Shih-Lei Ben LaiInstitute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.ORCID 0000-0002-1409-4701
Daniela PanákováLaboratory for Electrochemical Signaling in Development and Disease, Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany.ORCID 0000-0002-8739-6225
Didier Y R StainierDepartment of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.ORCID 0000-0002-0382-0026
Jan Philipp JunkerLaboratory for Quantitative Developmental Biology, Berlin Institute for Medical Systems Biology, Max Delbrück Center for Molecular Medicine in the Helmholtz Association, Berlin, Germany. janphilipp.junker@mdc-berlin.de.ORCID 0000-0002-2826-8290
Funding
Conditional genetics and precision genome editing resources for ZebrafishR24OD036201 · OD · IOWA STATE UNIVERSITY · PI KARL J CLARK, Stephen Carl Ekker · 2024 to 2026
$3.0M
Deutsche Forschungsgemeinschaft (German Research Foundation) 458913362Deutsches Zentrum für Herz-Kreislaufforschung (Deutsches Zentrum für Herz-Kreislaufforschung e.V.) 81X3100110Deutsches Zentrum für Herz-Kreislaufforschung (Deutsches Zentrum für Herz-Kreislaufforschung e.V.) 81Z0100103EC | EC Seventh Framework Programm | FP7 People: Marie-Curie Actions (FP7-PEOPLE - Specific Programme "People" Implementing the Seventh Framework Programme of the European Community for Research, Technological Development and Demonstration Activities (2007 to 2013)) 101106181 sc-LAB2FATEEC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council) 101021349-TaaGCEC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council) 101043364EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council) 694455-ZMODEuropean Molecular Biology Organization (EMBO) ALTF 972-2022Helmholtz Association ERC-RA-0047NIH HHS R24 OD036201ODCDC CDC HHS R24 OD036201
6 · The paper itself
Abstract
The adult zebrafish heart can regenerate after injury, but the earliest gene expression changes that trigger this process remain poorly understood. Here we show that in vivo single-cell RNA metabolic labeling, which marks newly made RNA in individual cells, can capture rapid responses in the adult zebrafish heart after injury. Within the first 6 h, we detect activation of innate immune programs, including Toll-like receptor signaling, in a subset of macrophage-like immune cells. Analysis of a larger single-cell dataset indicates that neutrophils also contribute to this early response. Guided by these data, we show that macrophage-specific inhibition of the Toll-like receptor adaptor MyD88 reduces the pro-inflammatory macrophage response at the injury site and improves early hallmarks of regeneration. Our work establishes RNA metabolic labeling as a useful approach for measuring acute responses in vivo at single-cell resolution and identifies early immune-cell activation as a tunable component of heart regeneration.
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.
In vivo single-cell RNA metabolic labeling resolves early transcriptional responders in the regenerating zebrafish heart. · full record | OpenQuestion