Evidence map›Paper›PMID 41396491›Full record

ArticleInflammation2025

Loss of the miR-221/222 Cluster Promotes the Pathogenesis of Osteoarthritis in Inflamed Mouse Chondrocytes and Osteoarthritis Models.

Xinlei Liu, Fangyu Feng, Yiman Jin, Chuang Ma, Qiaozhen Zhu, Yang You, Mengju Gao, Xinyu Li, Xinli Niu, Junpeng Wang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Inflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

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

1 citing paper in PubMed.

  1. Review
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

10 authors.

Xinlei LiuInfection and Immunity Institute and Translational Medical Center of Huaihe Hospital, Henan University, 115 Ximen Street, 475000, Kaifeng, China.
Fangyu FengInfection and Immunity Institute and Translational Medical Center of Huaihe Hospital, Henan University, 115 Ximen Street, 475000, Kaifeng, China.
Yiman JinInfection and Immunity Institute and Translational Medical Center of Huaihe Hospital, Henan University, 115 Ximen Street, 475000, Kaifeng, China.
Chuang MaInfection and Immunity Institute and Translational Medical Center of Huaihe Hospital, Henan University, 115 Ximen Street, 475000, Kaifeng, China.
Qiaozhen ZhuInfection and Immunity Institute and Translational Medical Center of Huaihe Hospital, Henan University, 115 Ximen Street, 475000, Kaifeng, China.
Yang YouInfection and Immunity Institute and Translational Medical Center of Huaihe Hospital, Henan University, 115 Ximen Street, 475000, Kaifeng, China.
Mengju GaoInfection and Immunity Institute and Translational Medical Center of Huaihe Hospital, Henan University, 115 Ximen Street, 475000, Kaifeng, China.
Xinyu LiInfection and Immunity Institute and Translational Medical Center of Huaihe Hospital, Henan University, 115 Ximen Street, 475000, Kaifeng, China.
Xinli NiuSchool of Life Science, Henan University, 1 Jinming Street, 475000, Kaifeng, China. niuxinli@henu.edu.cn.
Junpeng WangInfection and Immunity Institute and Translational Medical Center of Huaihe Hospital, Henan University, 115 Ximen Street, 475000, Kaifeng, China. jpwangchina@henu.edu.cn.

Funding

Natural Science Foundation of Henan Province 242300421292
6 · The paper itself

Abstract

Osteoarthritis (OA) is a degenerative joint disorder with the destruction of the joint's structural and functional which affects the entire joint. An important feature of OA is the progressive degeneration of articular cartilage due to an imbalance between extracellular matrix synthesis and degradation. While the molecular basis of OA remains unclear, microRNAs (miRNAs) have been recognized as key factors in controlling cartilage homeostasis and inflammation. Of these, miR-221 and miR-222 are implicated in inflammatory and degenerative disease, but their exact role in OA has yet to be determined. This study aims to assess the impact of miR-221/222 cluster knockout (KO) on mouse OA models and to explore its underlying mechanisms. OA was induced in miR-221/222 KO mice utilizing the destabilization of the medial meniscus (DMM) model. Joint pathology was examined by X-ray, histological scoring, immunofluorescence, and biochemical assays. In addition, in vitro studies were performed using IL-1β-treated chondrocytes. Gain-of-function experiments were performed using miR-221/222 agomir. OA tissues of mice and mouse primary chondrocytes treated with IL-1β showed a decrease in miR-221 and miR-222 expression as compared with the shamed mice. However, miR-221/222 KO mice exhibited significant osteophyte formation and cartilage degradation, with a marked increase in collagen I, MMP-13 levels, and a significant decrease in COL2A1 levels. In vitro, miR-221/222 KO led to increased inflammatory mediators like IL-6 and TNF-α, which promoted chondrocyte apoptosis and activated the MAPK signaling pathway, thereby exacerbating OA progression. Conversely, treatment with miR-221/222 agomir attenuated OA progression in vivo. These findings suggest that loss of the miR-221 cluster contributes to OA progression by promoting inflammation, apoptosis, and matrix degradation, partly through MAPK signaling. Restoring miR-221/222 may hold therapeutic potential, but human studies are needed for validation.

Indexed as

ChondrocytesMicroRNAsOsteoarthritisAnimalsApoptosisCells, CulturedDisease Models, AnimalInflammationMiceMice, KnockoutMicroRNAsMIRN221 microRNA, mouseMIRN222 microRNA, mouseApoptosisInflammationMAPK signalsMiRNAsOsteoarthritis

Identifiers

PMID41396491
PMCPMC12705854

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LicenceCC BY-NC-ND
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Registered trials

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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.