Evidence map›Paper›PMID 37007968›Full record

ReviewFrontiers in genetics2023

Tenascin-X as a causal gene for classical-like Ehlers-Danlos syndrome.

Emiko Okuda-Ashitaka, Ken-Ichi Matsumoto

Open access · goldFull text readReview
In one paragraph

Review in Frontiers in genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
5.3field-weighted citation impact, top 4% of its field
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

12 citing papers in PubMed, 17 citations in OpenAlex.

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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

2 authors at 2 institutions in 1 country.

Emiko Okuda-AshitakaDepartment of Biomedical Engineering, Osaka Institute of Technology, Osaka, Japan.
Ken-Ichi MatsumotoDepartment of Biosignaling and Radioisotope Experiment, Interdisciplinary Center for Science Research, Head Office for Research and Academic Information, Shimane University, Izumo, Japan.
Osaka Institute of Technology · JPShimane University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tenascin-X (TNX) is an extracellular matrix glycoprotein for which a deficiency results in a recessive form of classical-like Ehlers-Danlos syndrome (clEDS), a heritable connective tissue disorder with hyperextensible skin without atrophic scarring, joint hypermobility, and easy bruising. Notably, patients with clEDS also suffer from not only chronic joint pain and chronic myalgia but also neurological abnormalities such as peripheral paresthesia and axonal polyneuropathy with high frequency. By using TNX-deficient (

Indexed as

clEDSEhlers-Danlos syndromesfibrosispaintenascin-Xtumor suppressor

Identifiers

PMID37007968
PMCPMC10050494
OpenAlexW4324375437

What OpenQuestion holds

Textfull text, public
LicenceCC BY
reference markers read5
measurements read42
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.