Evidence map›Paper›PMID 38644475›Full record

ArticleJournal of nanobiotechnology2024

Macrophage-derived mir-100-5p orchestrates synovial proliferation and inflammation in rheumatoid arthritis through mTOR signaling.

Huan Liu, Yuehong Chen, Yupeng Huang, Ling Wei, Jingjing Ran, Qianwei Li, Yunru Tian, Zhongling Luo, Leiyi Yang, Hongjiang Liu and 2 more

Abstract read
In one paragraph

Article in Journal of nanobiotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

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  10. mTOR Signaling in Macrophages: All Depends on the Context.International journal of molecular sciences · 2025
    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

12 authors.

Huan LiuDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, 610041, China.
Yuehong ChenDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, 610041, China.
Yupeng HuangDepartment of General Practice, West China Hospital, General Practice Medical Center, Sichuan University, Chengdu, 610041, China.
Ling WeiHospital of Chengdu Office of People's Government of Tibetan Autonomous region, Chengdu, 610041, China.
Jingjing RanDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, 610041, China.
Qianwei LiDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, 610041, China.
Yunru TianDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, 610041, China.
Zhongling LuoDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, 610041, China.
Leiyi YangDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, 610041, China.
Hongjiang LiuDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, 610041, China.
Geng YinDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, 610041, China. yingeng1975@163.com.
Qibing XieDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, 610041, China. xieqibing1971@163.com.

Funding

Sichuan Province Science and Technology Support Program 2021JDRC0045Sichuan Province Science and Technology Support Program 2021JDRC0169Sichuan Province Science and Technology Support Program 2021YFS0164the 1.3.5 Project for Disciplines of Excellence, West China Hospital, Sichuan University ZYJC21024the Clinical Research Incubation Project of West China Hospital, Sichuan University 2019HXFH038the Clinical Research Incubation Project of West China Hospital, Sichuan University 2021HXFH018
6 · The paper itself

Abstract

backgroundRheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by synovial inflammation, causing substantial disability and reducing life quality. While macrophages are widely appreciated as a master regulator in the inflammatory response of RA, the precise mechanisms underlying the regulation of proliferation and inflammation in RA-derived fibroblast-like synoviocytes (RA-FLS) remain elusive. Here, we provide extensive evidence to demonstrate that macrophage contributes to RA microenvironment remodeling by extracellular vesicles (sEVs) and downstream miR-100-5p/ mammalian target of rapamycin (mTOR) axis.

resultsWe showed that bone marrow derived macrophage (BMDM) derived-sEVs (BMDM-sEVs) from collagen-induced arthritis (CIA) mice (cBMDM-sEVs) exhibited a notable increase in abundance compared with BMDM-sEVs from normal mice (nBMDM-sEVs). cBMDM-sEVs induced significant RA-FLS proliferation and potent inflammatory responses. Mechanistically, decreased levels of miR-100-5p were detected in cBMDM-sEVs compared with nBMDM-sEVs. miR-100-5p overexpression ameliorated RA-FLS proliferation and inflammation by targeting the mTOR pathway. Partial attenuation of the inflammatory effects induced by cBMDM-sEVs on RA-FLS was achieved through the introduction of an overexpression of miR-100-5p.

conclusionsOur work reveals the critical role of macrophages in exacerbating RA by facilitating the transfer of miR-100-5p-deficient sEVs to RA-FLS, and sheds light on novel disease mechanisms and provides potential therapeutic targets for RA interventions.

Indexed as

Arthritis, RheumatoidMacrophagesMicroRNAsSignal TransductionTOR Serine-Threonine KinasesAnimalsArthritis, ExperimentalCell ProliferationExtracellular VesiclesHumansInflammationMaleMiceMice, Inbred DBASynovial MembraneSynoviocytesMicroRNAsMirn100 microRNA, mousemTOR protein, mouseTOR Serine-Threonine KinasesExtracellular vesiclesMacrophagesmiR-100-5pmTORRheumatoid arthritis

Identifiers

PMID38644475
PMCPMC11034106

What Socratic 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 Socratic graph.