Evidence map›Paper›PMID 33099538›Full record

ArticleAging2020

Down-regulated ciRS-7/up-regulated miR-7 axis aggravated cartilage degradation and autophagy defection by PI3K/AKT/mTOR activation mediated by IL-17A in osteoarthritis.

Xindie Zhou, Jin Li, Yuanshuai Zhou, Zhicheng Yang, Haoyu Yang, Dong Li, Junjie Zhang, Yi Zhang, Nanwei Xu, Yong Huang and 1 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
11.6field-weighted citation impact, top 1% 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

58 citing papers in PubMed, 92 citations in OpenAlex.

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  16. Chondrocyte autophagy mechanism and therapeutic prospects in osteoarthritis.Frontiers in cell and developmental biology · 2024
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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

11 authors at 5 institutions in 1 country.

Xindie ZhouDepartment of Orthopedics, The Affiliated Changzhou No.2 People’s Hospital of Nanjing Medical University, Changzhou 213000, China.
Jin LiDepartment of Orthopedic Surgery, The Second Affiliated Hospital of Jiaxing University, Jiaxing 314000, China.
Yuanshuai ZhouSuzhou Institute of Biomedical Engineering and Technology, Chinese Academy of Sciences, Suzhou 215000, China.
Zhicheng YangDepartment of Orthopedics, The Affiliated Changzhou No.2 People’s Hospital of Nanjing Medical University, Changzhou 213000, China.
Haoyu YangDepartment of Orthopedics, The Affiliated Changzhou No.2 People’s Hospital of Nanjing Medical University, Changzhou 213000, China.
Dong LiDepartment of Orthopedics, The Affiliated Changzhou No.2 People’s Hospital of Nanjing Medical University, Changzhou 213000, China.
Junjie ZhangDepartment of Orthopedics, The Affiliated Changzhou No.2 People’s Hospital of Nanjing Medical University, Changzhou 213000, China.
Yi ZhangDepartment of Orthopedics, The Affiliated Changzhou No.2 People’s Hospital of Nanjing Medical University, Changzhou 213000, China.
Nanwei XuDepartment of Orthopedics, The Affiliated Changzhou No.2 People’s Hospital of Nanjing Medical University, Changzhou 213000, China.
Yong HuangDepartment of Orthopedics, The Affiliated Changzhou No.2 People’s Hospital of Nanjing Medical University, Changzhou 213000, China.
Lifeng JiangDepartment of Orthopedic Surgery, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310000, China.
Changzhou No.2 People's Hospital · CNNanjing Medical University · CNJiaxing University · CNSecond Affiliated Hospital of Zhejiang University · CNSuzhou Institute of Biomedical Engineering and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoarthritis (OA) is one of the most painful and widespread chronic degenerative joint diseases and is characterized by destructed articular cartilage and inflamed joints. Previously, our findings indicated that circular RNA ciRS-7 (ciRS-7)/microRNA 7 (miR-7) axis is abnormally expressed in OA, and regulates proliferation, inflammatory responses, and apoptosis of interleukin-1β (IL-1β)-stimulated chondrocytes. However, its underlying role in OA remains unknown. In this study, we first validated cartilage degradation and defection of autophagy in samples of OA patients. IL-1β initially stimulated autophagy of chondrocytes, and ultimately significantly suppressed autophagy. Upregulated ciRS-7/down-regulated miR-7 aggravated IL-1β-induced cartilage degradation, and restrained autophagy

Indexed as

AutophagyAnimalsCartilage, ArticularCase-Control StudiesCell LineChondrocytesDisease Models, AnimalGene Expression RegulationHumansInterleukin-17Interleukin-1betaMaleMicroRNAsOsteoarthritisPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktIL17A protein, humanInterleukin-17Interleukin-1betalong non-coding RNA CDR1AS, humanMicroRNAsMIRN7-1 microRNA, humanMIRN7-1 microRNA, ratMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Long NoncodingTOR Serine-Threonine KinasesautophagyciRS-7IL-17AmiR-7osteoarthritis

Identifiers

PMID33099538
PMCPMC7655186
OpenAlexW3093930855

What OpenQuestion 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 OpenQuestion graph.