Evidence map›Paper›PMID 35003796›Full record

Trial reportJournal of advanced research2022

Cartilage degeneration is associated with activation of the PI3K/AKT signaling pathway in a growing rat experimental model of developmental trochlear dysplasia.

Wei Lin, Huijun Kang, Yingzhen Niu, Jinghui Niu, Chongyi Fan, Xunkai Feng, Fei Wang

Open access · goldAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Journal of advanced research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.6field-weighted citation impact, top 38% 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

13 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
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  3. Three-dimensionally-printed biphasic PCL/Regenerative biomaterials · 2026
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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

7 authors at 1 institution in 1 country.

Wei LinThird Hospital of Hebei Medical University, Shijiazhuang, Hebei 050051, China.
Huijun KangThird Hospital of Hebei Medical University, Shijiazhuang, Hebei 050051, China.
Yingzhen NiuThird Hospital of Hebei Medical University, Shijiazhuang, Hebei 050051, China.
Jinghui NiuThird Hospital of Hebei Medical University, Shijiazhuang, Hebei 050051, China.
Chongyi FanThird Hospital of Hebei Medical University, Shijiazhuang, Hebei 050051, China.
Xunkai FengThird Hospital of Hebei Medical University, Shijiazhuang, Hebei 050051, China.
Fei WangThird Hospital of Hebei Medical University, Shijiazhuang, Hebei 050051, China.
Hebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Trochlear dysplasia is a commonly encountered lower extremity deformity in humans. However, the molecular mechanism of cartilage degeneration in trochlear dysplasia is unclear thus far. Objectives: The PI3K/AKT signaling pathway is known to be important for regulating the pathophysiology of cartilage degeneration. The aim of this study was to investigate the relationship of the PI3K/AKT signaling pathway with trochlear dysplasia cartilage degeneration. Methods: In total, 120 female Sprague-Dawley rats (4 weeks of age) were randomly separated into control and experimental groups. Distal femurs were isolated from the experimental group at 4, 8, and 12 weeks after surgery; they were isolated from the control group at the same time points. Micro-computed tomography and histological examination were performed to investigate trochlear anatomy and changes in trochlear cartilage. Subsequently, expression patterns of PI3K/AKT, TGFβ1, and ADAMTS-4 in cartilage were investigated by immunohistochemistry and quantitative polymerase chain reaction. Results: In the experimental group, the trochlear dysplasia model was successfully established at 8 weeks after surgery. Moreover, cartilage degeneration was observed beginning at 8 weeks after surgery, with higher protein and mRNA expression levels of PI3K/AKT, TGFβ1, and ADAMTS-4, relative to the control group. Conclusion: Patellar instability might lead to trochlear dysplasia in growing rats. Moreover, trochlear dysplasia may cause patellofemoral osteoarthritis; cartilage degeneration in trochlear dysplasia might be associated with activation of the PI3K/AKT signaling pathway. These results provide insights regarding the high incidence of osteoarthritis in patients with trochlear dysplasia. However, more research is needed to clarify the underlying mechanisms.

Indexed as

Joint InstabilityPatellofemoral JointAnimalsFemaleHumansModels, TheoreticalPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleySignal TransductionX-Ray MicrotomographyPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktCartilage degenerationOsteoarthritisPatellar instabilityPI3K/AKTTrochlear dysplasia

Identifiers

PMID35003796
PMCPMC8721235
OpenAlexW3154430421

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.