Evidence map›Paper›PMID 35563063›Full record

ReviewInternational journal of molecular sciences2022

Regulatory Mechanisms of

Yoshifumi Takahata, Hiromasa Hagino, Ayaka Kimura, Mitsuki Urushizaki, Shiori Yamamoto, Kanta Wakamori, Tomohiko Murakami, Kenji Hata, Riko Nishimura

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 2 pooled it
7.1field-weighted citation impact, top 2% 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

28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 44 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

9 authors at 1 institution in 1 country.

Yoshifumi TakahataDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, 1-8 Yamadaoka Suita, Osaka 565-0871, Japan.ORCID 0000-0002-3322-0515
Hiromasa HaginoDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, 1-8 Yamadaoka Suita, Osaka 565-0871, Japan.
Ayaka KimuraDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, 1-8 Yamadaoka Suita, Osaka 565-0871, Japan.
Mitsuki UrushizakiDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, 1-8 Yamadaoka Suita, Osaka 565-0871, Japan.
Shiori YamamotoDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, 1-8 Yamadaoka Suita, Osaka 565-0871, Japan.
Kanta WakamoriDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, 1-8 Yamadaoka Suita, Osaka 565-0871, Japan.
Tomohiko MurakamiDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, 1-8 Yamadaoka Suita, Osaka 565-0871, Japan.ORCID 0000-0002-5021-5494
Kenji HataDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, 1-8 Yamadaoka Suita, Osaka 565-0871, Japan.
Riko NishimuraDepartment of Molecular and Cellular Biochemistry, Osaka University Graduate School of Dentistry, 1-8 Yamadaoka Suita, Osaka 565-0871, Japan.
The University of Osaka · JP

Funding

Ministry of Education, Culture, Sports, Science and Technology 21K09827,21H04841,20K20475
6 · The paper itself

Abstract

Owing to the rapid aging of society, the numbers of patients with joint disease continue to increase. Accordingly, a large number of patients require appropriate treatment for osteoarthritis (OA), the most frequent bone and joint disease. Thought to be caused by the degeneration and destruction of articular cartilage following persistent and excessive mechanical stimulation of the joints, OA can significantly impair patient quality of life with symptoms such as knee pain, lower limb muscle weakness, or difficulty walking. Because articular cartilage has a low self-repair ability and an extremely low proliferative capacity, healing of damaged articular cartilage has not been achieved to date. The current pharmaceutical treatment of OA is limited to the slight alleviation of symptoms (e.g., local injection of hyaluronic acid or non-steroidal anti-inflammatory drugs); hence, the development of effective drugs and regenerative therapies for OA is highly desirable. This review article summarizes findings indicating that proteoglycan 4 (

Indexed as

Cartilage, ArticularOsteoarthritisAnimalsChondrocytesGrowth Differentiation Factor 5HumansMiceProteoglycan 4ProteoglycansQuality of LifeGDF5 protein, humanGdf5 protein, mouseGrowth Differentiation Factor 5PRG4 protein, humanPrg4 protein, mouseProteoglycan 4ProteoglycansEGFRosteoarthritisPrg4TGF-βTranscription factorWntβ-catenin

Identifiers

PMID35563063
PMCPMC9105027
OpenAlexW4224225611

What Socratic holds

Textmetadata
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 Socratic graph.