Evidence map›Paper›PMID 40155964›Full record

ArticleJournal of orthopaedic surgery and research2025

MiR-103-3p regulates chondrocyte autophagy, apoptosis, and ECM degradation through the PI3K/Akt/mTOR pathway by targeting CPEB3.

Jun Li, Farui Sun, Yuanjin Zhang, Xian Pan, Bo Li, Guofu Zhang, Qian Zhou

Abstract read
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In one paragraph

Article in Journal of orthopaedic surgery and research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

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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

7 citing papers in PubMed.

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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.

Jun LiDepartment of Orthopedics, Huangshi Central Hospital, Affiliated Hospital of Hubei Polytechnic University, Hungshi, 435000, China.
Farui SunDepartment of Orthopedics, Huangshi Central Hospital, Affiliated Hospital of Hubei Polytechnic University, Hungshi, 435000, China.
Yuanjin ZhangDepartment of Orthopedics, Huangshi Central Hospital, Affiliated Hospital of Hubei Polytechnic University, Hungshi, 435000, China.
Xian PanDepartment of Orthopedics, Huangshi Central Hospital, Affiliated Hospital of Hubei Polytechnic University, Hungshi, 435000, China.
Bo LiDepartment of Orthopedics, Huangshi Central Hospital, Affiliated Hospital of Hubei Polytechnic University, Hungshi, 435000, China.
Guofu ZhangDepartment of Orthopedics, Huangshi Central Hospital, Affiliated Hospital of Hubei Polytechnic University, Hungshi, 435000, China.
Qian ZhouDepartment of Geriatrics, Huangshi Central Hospital, Affiliated Hospital of Hubei Polytechnic University, Tianjin Avenue No. 141, Huangshigang District, 435000, Hungshi, Hubei Province, China. qzhoudoctor@hotmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChondrocyte apoptosis is associated with the severity of cartilage destruction and matrix degeneration in the progression of osteoarthritis. Increasing evidence indicates that autophagy has a significant cytoprotective effect against chondrocyte apoptosis. Here, we investigated the role of microRNA-103-3p (miR-103-3p) in regulating chondrocyte function and elucidated the underlying mechanism.

methodsMiR-103-3p expression in interleukin-1β (IL-1β)-stimulated chondrocytes was evaluated using RT-qPCR. The targets of miR-103-3p predicted by online databases were verified using biotin-based pulldown assay and luciferase reporter assay. IL-1β stimulated-chondrocytes were transfected with miR-103-3p inhibitor along with siRNA targeting cytoplasmic polyadenylation element-binding protein3 (siCPEB3), the autophagy inhibitor 3-MA, or the PI3K agonist 740 Y-P. Chondrocyte proliferation was evaluated using cell counting kit-8. Apoptosis was detected by flow cytometry. The levels of apoptosis-, extracellular matrix (ECM)-, autophagy-, and the PI3K/Akt/mTOR pathway-related proteins in chondrocytes were detected using immunoblotting or immunofluorescence.

resultsWe found that IL-1β stimulation upregulated miR-103-3p and downregulated CPEB3 in mouse chondrocytes. Inhibiting miR-103-3p reduced IL-1β-induced apoptosis and ECM macromolecule degradation while enhancing autophagy in chondrocytes. MiR-103-3p targeted CPEB3, and its downregulation rescued the expression of level in IL-1β stimulated-chondrocytes. MiR-103-3p downregulation inhibited the PI3K/Akt/mTOR pathway in IL-1β stimulated-chondrocytes by upregulating CPEB3. 3-MA, 740 Y-P, or CPEB3 knockdown counteracted the effect of miR-103-3p downregulation on chondrocyte apoptosis, ECM macromolecule degradation, and autophagy.

conclusionOverall, inhibition of miR-103-3p reduces IL-1β-induced apoptosis and ECM macromolecule degradation in chondrocytes by enhancing autophagy through the CPEB3/PI3K/Akt/mTOR pathway.

Indexed as

ApoptosisAutophagyChondrocytesExtracellular MatrixMicroRNAsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA-Binding ProteinsTOR Serine-Threonine KinasesAnimalsCells, CulturedHumansInterleukin-1betaMiceOsteoarthritisSignal TransductionInterleukin-1betaMicroRNAsMIRN103 microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA-Binding ProteinsTOR Serine-Threonine KinasesAutophagyChondrocyteCPEB3miR-103-3pOsteoarthritisPI3K

Identifiers

PMID40155964
PMCPMC11954267

What Socratic holds

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LicenceCC BY-NC-ND
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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.