Evidence map›Paper›PMID 29636866›Full record

ArticleAmerican journal of translational research2018

Protective effects of PI3K/Akt signal pathway induced cell autophagy in rat knee joint cartilage injury.

Qingbin Zhang, Shixiang Lai, Xunyao Hou, Wei Cao, Ying Zhang, Zhaoqiang Zhang

Open access · greenAbstract read
In one paragraph

Article in American journal of translational research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

33 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
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  14. Effects of Prunus Tomentosa Thumb Total Flavones on adjuvant arthritis in rats and regulation of autophagy.Technology and health care : official journal of the European Society for Engineering and Medicine · 2023
    Article
  15. Review
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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

6 authors at 3 institutions in 1 country.

Qingbin ZhangTemporomandibular Joint Department, Stomatology Hospital of Guangzhou Medical UniversityGuangzhou 510140, Guangdong, China.
Shixiang LaiKey Laboratory of Oral Medicine, Guangzhou Institute of Oral DiseaseGuangzhou 510140, Guangdong, China.
Xunyao HouDepartment of Senile Neurology, Shandong Provincial Hospital Affiliated to Shandong University324#, Jing Wu Road, Jinan 250021, China.
Wei CaoTemporomandibular Joint Department, Stomatology Hospital of Guangzhou Medical UniversityGuangzhou 510140, Guangdong, China.
Ying ZhangTemporomandibular Joint Department, Stomatology Hospital of Guangzhou Medical UniversityGuangzhou 510140, Guangdong, China.
Zhaoqiang ZhangMaxillofacial Surgery Department, Stomatology Hospital of Southern Medical UniversityGuangzhou 510260, Guangdong, China.
Stomatology Hospital · CNKey Laboratory of Guangdong Province · CNShandong Provincial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As the major reason for limb dysfunction, osteoarthritis (OA) is closely correlated with the level of cellular autophagy. PI3K/Akt is a classical signaling pathway which regulates autophagy, but with unclear roles in OA related cartilage injury. Studying PI3K/Akt induced autophagy in rat knee joint cartilage injury and possible functional mechanism is of critical importance for clinical treatment. This study established a rat knee joint cartilage injury model, in which Akt agonist IGF-1 or autophagy inducer Rapamycin was administrated. Western blot was used to detect the expression level of AKT, phosphorylated AKT, Beclin-1 and LC3-II/I. Formation of autophagosome and lysosome was assessed by transmission electron microscopy. HE, safranin O and toluidine blue staining was used to evaluate cartilage injury. TUNEL staining was performed to measure cell apoptosis. Real-time quantitative PCR measured the expression of cartilage injury indexes such as Aggrecan, Collagen II and MMP13. Compared with normal group, iodacetic acid treatment group showed cartilage injury, whereas AKT activation and autophagy induction groups had significant improvement. mRNA analysis showed enhanced degradation of Aggrecan and Collagen II in AKT activation and autophagy groups with decreased MMP13 mRNA level (P<0.05). Western blot results showed that after AKT activation and autophagy induction, protein levels of Beclin-1 and LC3-II/I were remarkably elevated (P<0.05). TUNEL assay showed significant inhibition of cell apoptosis. In conclusion, activation of PI3K/Akt signal pathway can improve iodacetic acid induced rat knee joint cartilage injury through inducing cell autophagy.

Indexed as

cell autophagyOsteoarthritis cartilage injuryPI3K/Akt signaling pathway

Identifiers

PMID29636866
PMCPMC5883117
OpenAlexW2905038803

What OpenQuestion holds

Textmetadata
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.