Evidence map›Paper›PMID 39480704›Full record

ArticleeLife2024

A Pvr-AP-1-Mmp1 signaling pathway is activated in astrocytes upon traumatic brain injury.

Tingting Li, Wenwen Shi, Margaret S Ho, Yong Q Zhang

Abstract read
In one paragraph

Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. ALife science alliance · 2025
    Article
  6. Review
  7. Article
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

4 authors.

Tingting LiKey Laboratory of Molecular and Developmental Biology, Institute of Genetics and Developmental Biology, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Beijing, China.ORCID https://orcid.org/0000-0003-1309-036X
Wenwen ShiKey Laboratory of Molecular and Developmental Biology, Institute of Genetics and Developmental Biology, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Beijing, China.
Margaret S HoInstitute of Neuroscience, National Yang Ming Chiao Tung University, Taipei, Taiwan.ORCID https://orcid.org/0000-0002-2387-7564
Yong Q ZhangKey Laboratory of Molecular and Developmental Biology, Institute of Genetics and Developmental Biology, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Beijing, China.ORCID https://orcid.org/0000-0003-0581-4882

Funding

Chinese Academy of Sciences Strategic Priority Research Program B XDBS1020100Ministry of Education (MOE) in Taiwan Higher Education Sprout ProjectMinistry of Science and Technology of China 2019YFA0707100Ministry of Science and Technology of China 2021ZD0203900National Science and Technology Council Taiwan 113-2628-B-A49-007National Science Foundation of China 31830036National Science Foundation of China 31861143031National Science Foundation of China 31921002National Science Foundation of China 32170962
6 · The paper itself

Abstract

Traumatic brain injury (TBI) caused by external mechanical forces is a major health burden worldwide, but the underlying mechanism in glia remains largely unclear. We report herein that

Indexed as

AstrocytesBrain Injuries, TraumaticDrosophila ProteinsMatrix Metalloproteinase 1Signal TransductionTranscription Factor AP-1AnimalsDrosophila melanogasterReceptor Protein-Tyrosine KinasesDrosophila ProteinsMatrix Metalloproteinase 1Receptor Protein-Tyrosine KinasesTranscription Factor AP-1astrocytesD. melanogasterDrosophilamatrix metalloproteinaseneurosciencePvrRNA-seqtraumatic brain injury

Identifiers

PMID39480704
PMCPMC11527428

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.