Evidence map›Paper›PMID 33627637›Full record

ArticleCell death discovery2021

Exosomes derived from miR-126-3p-overexpressing synovial fibroblasts suppress chondrocyte inflammation and cartilage degradation in a rat model of osteoarthritis.

Yan Zhou, Jianghua Ming, Yaming Li, Bochun Li, Ming Deng, Yonggang Ma, Zhonghui Chen, Yubiao Zhang, Jia Li, Shiqing Liu

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
6.6field-weighted citation impact, top 2% 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

80 citing papers in PubMed, 104 citations in OpenAlex.

  1. Review
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  7. From pathogenesis to therapy: extracellular vesicles in osteoarthritis.Frontiers in bioengineering and biotechnology · 2026
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  11. Exosomes: critical mediator and therapeutic target for osteoarthritis.American journal of translational research · 2026
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20 more citing papers are in PubMed but not listed here.

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 at 3 institutions in 1 country.

Yan ZhouDepartment of Orthopedics, Renmin Hospital of Wuhan University, Wuhan, China. yanzhou0827@whu.edu.cn.ORCID http://orcid.org/0000-0002-1328-8408
Jianghua MingDepartment of Orthopedics, Renmin Hospital of Wuhan University, Wuhan, China.
Yaming LiDepartment of Orthopedics, Renmin Hospital of Wuhan University, Wuhan, China.
Bochun LiDepartment of Acupuncture, Wuhan Union Hospital, Huazhong University of Science and Technology, Wuhan, China.
Ming DengCentral Laboratory, Renmin Hospital of Wuhan University, Wuhan, China.
Yonggang MaDepartment of Orthopedics, Renmin Hospital of Wuhan University, Wuhan, China.
Zhonghui ChenCentral Laboratory, Renmin Hospital of Wuhan University, Wuhan, China.
Yubiao ZhangCentral Laboratory, Renmin Hospital of Wuhan University, Wuhan, China.
Jia LiCollege of Acupuncture and Bone Injury, Hubei University of Traditional Chinese Medicine, Wuhan, China.
Shiqing LiuDepartment of Orthopedics, Renmin Hospital of Wuhan University, Wuhan, China.
Wuhan University · CNHubei University of Chinese Medicine · CNWuhan Union Hospital · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81802203
6 · The paper itself

Abstract

MicroRNAs (miRNAs) encapsulated within exosomes can serve as essential regulators of intercellular communication and represent promising biomarkers of several aging-associated disorders. However, the relationship between exosomal miRNAs and osteoarthritis (OA)-related chondrocytes and synovial fibroblasts (SFCs) remain to be clarified. Herein, we profiled synovial fluid-derived exosomal miRNAs and explored the effects of exosomal miRNAs derived from SFCs on chondrocyte inflammation, proliferation, and survival, and further assessed their impact on cartilage degeneration in a surgically-induced rat OA model. We identified 19 miRNAs within synovial fluid-derived exosomes that were differentially expressed when comparing OA and control patients. We then employed a microarray-based approach to confirm that exosomal miRNA-126-3p expression was significantly reduced in OA patient-derived synovial fluid exosomes. At a functional level, miRNA-126-3p mimic treatment was sufficient to promote rat chondrocyte migration and proliferation while also suppressing apoptosis and IL-1β, IL-6, and TNF-α expression. SFC-miRNA-126-3p-Exos were able to suppress apoptotic cell death and associated inflammation in chondrocytes. Our in vivo results revealed that rat SFC-derived exosomal miRNA-126-3p was sufficient to suppress the formation of osteophytes, prevent cartilage degeneration, and exert anti-apoptotic and anti-inflammatory effects on articular cartilage. Overall, our findings indicate that SFC exosome-delivered miRNA-126-3p can constrain chondrocyte inflammation and cartilage degeneration. As such, SFC-miRNA-126-3p-Exos may be of therapeutic value for the treatment of patients suffering from OA.

Identifiers

PMID33627637
PMCPMC7904758
OpenAlexW3131918383

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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.