Real-time imaging of blood coagulation and angiogenesis during development in a zebrafish model of type I antithrombin deficiency.

Yuta Imai, Satoru Ozaki, Taiki Noda, Isao Kobayashi, Kayo Sugitani, Satomi Kasashima, Eriko Morishita, Yuhei Araiso

Abstract read

In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it

0cells of the map it votes in

0citing 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

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

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

8 authors.

Yuta ImaiDepartment of Clinical Laboratory Science, Division of Health Sciences, Graduate School of Medical Sciences, Kanazawa University, 5-11-80 Kodatsuno, Kanazawa, Ishikawa, 920-0942, Japan.

Satoru OzakiDepartment of Clinical Laboratory Science, Division of Health Sciences, Graduate School of Medical Sciences, Kanazawa University, 5-11-80 Kodatsuno, Kanazawa, Ishikawa, 920-0942, Japan.

Taiki NodaDepartment of Clinical Laboratory Science, Division of Health Sciences, Graduate School of Medical Sciences, Kanazawa University, 5-11-80 Kodatsuno, Kanazawa, Ishikawa, 920-0942, Japan.

Isao KobayashiFaculty of Biological Science and Technology, Institute of Science and Engineering, Kanazawa University, Kanazawa, Ishikawa, Japan.

Kayo SugitaniDepartment of Clinical Laboratory Science, Division of Health Sciences, Graduate School of Medical Sciences, Kanazawa University, 5-11-80 Kodatsuno, Kanazawa, Ishikawa, 920-0942, Japan.

Satomi KasashimaDepartment of Clinical Laboratory Science, Division of Health Sciences, Graduate School of Medical Sciences, Kanazawa University, 5-11-80 Kodatsuno, Kanazawa, Ishikawa, 920-0942, Japan.

Eriko MorishitaDepartment of Clinical Laboratory Science, Division of Health Sciences, Graduate School of Medical Sciences, Kanazawa University, 5-11-80 Kodatsuno, Kanazawa, Ishikawa, 920-0942, Japan. eriko86@staff.kanazawa-u.ac.jp.

Yuhei AraisoDepartment of Clinical Laboratory Science, Division of Health Sciences, Graduate School of Medical Sciences, Kanazawa University, 5-11-80 Kodatsuno, Kanazawa, Ishikawa, 920-0942, Japan. araiso@staff.kanazawa-u.ac.jp.

Funding

Japan Science and Technology Agency JPMJFR200FJapan Science and Technology Agency JPMJSP2135

6 · The paper itself

Abstract

Severe type I antithrombin (AT) deficiency is considered to cause embryonic lethality. Although several pathological analyses using mice or zebrafish have been attempted, the previous studies did not unveil the detailed mechanism leading to lethality in the early developmental stage. In order to solve this problem, we established type I AT deficient zebrafish by the CRISPR/Cas9 system into Tg(gata1:dsRed) and Tg(fli1a:GFP) lines, so that we could conduct real-time imaging of thrombosis and angiogenesis using fluorescence stereo zoom microscopy. The established zebrafish AT (zAT) mutants harbored frameshift mutations which resulted to be type I AT deficient, unable to secrete zAT protein into blood. Both heterozygous (zAT

Indexed as

Blood CoagulationNeovascularization, PhysiologicZebrafishAngiogenesisAnimalsAnimals, Genetically ModifiedCRISPR-Cas SystemsDisease Models, AnimalThrombosisZebrafish ProteinsZebrafish ProteinsAngiogenesisAntithrombin deficiencyGenome editingThrombosisZebrafish

Identifiers

PMID40425635

DOI10.1038/s41598-025-01658-z

PMCPMC12117160

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LicenceCC BY-NC-ND

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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.