Evidence map›Paper›PMID 40068094›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

M6A Modified miR-31-5p Suppresses M1 Macrophage Polarization and Autoimmune Dry Eye by Targeting P2RX7.

Lu Zhao, Xuejia Li, Min Gao, Lin Liu, Binyun Ma, Xun Liu, Jiachen Zhang, Ruoxuan Liu, Bei Du, Ruihua Wei and 1 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. FTO-dependent mInflammation · 2026
    Article
  5. Review
  6. Review
  7. Exosomes in ocular graft-versus-host disease: an overview.International journal of ophthalmology · 2026
    Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
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.

Lu ZhaoTianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin, 300384, China.
Xuejia LiTianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin, 300384, China.
Min GaoTianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin, 300384, China.
Lin LiuTianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin, 300384, China.
Binyun MaDepartment of Medicine/Hematology, Keck School of Medicine of the University of Southern California, Los Angeles, CA, 90033, USA.
Xun LiuTianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin, 300384, China.
Jiachen ZhangTianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin, 300384, China.
Ruoxuan LiuTianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin, 300384, China.
Bei DuTianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin, 300384, China.
Ruihua WeiTianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin, 300384, China.ORCID https://orcid.org/0000-0002-9708-0355
Hong NianTianjin Key Laboratory of Retinal Functions and Diseases, Tianjin Branch of National Clinical Research Center for Ocular Disease, Eye Institute and School of Optometry, Tianjin Medical University Eye Hospital, Tianjin, 300384, China.

Funding

National Natural Science Foundation of China 81970793National Natural Science Foundation of China 82070929The Science & Technology Development Fund of Tianjin Education Commission for Higher Education 2023ZD018Tianjin Key Medical Discipline (Specialty) Construction Project TJYXZDXK-037ATianjin Medical University Eye Hospital High-Level innovative Talents Programme YDYYRCXM-B2023-3
6 · The paper itself

Abstract

The dysregulation of the M1/M2 macrophage balance plays a pivotal role in autoimmune diseases. However, the interplay between microRNAs (miRNAs) and N6-methyladenosine (m6A) modulation in regulating this balance remains poorly understood. Here, a significant reduction in miR-31-5p levels is observed in the lacrimal glands of rabbit autoimmune dacryoadenitis and the peripheral blood mononuclear cells (PBMCs) of Sjögren's syndrome (SS) dry eye patients. Overexpression of miR-31-5p exhibits preventive and therapeutic effects on rabbit autoimmune dacryoadenitis. Further investigation revealed that miR-31-5p overexpression significantly restored the M1/M2 macrophage balance both in vivo and in vitro. Mechanistically, miR-31-5p directly targets the P2x7 receptor (P2RX7), leading to the inactivation of p38 mitogen-activated protein kinases (MAPK) signaling and reduced expression of M1 markers. Furthermore, methylated RNA immunoprecipitation and luciferase reporter assays demonstrated that fat mass and obesity-associated protein (FTO)-mediated m6A demethylation, which sustains pri-miR-31 stability, is responsible for the decreased miR-31-5p levels in autoimmune dry eye. Notably, PBMC samples from SS dry eye patients further support the link between reduced miR-31-5p levels and M1 macrophage activation observed in rabbits. Overall, these data highlight the critical role of the FTO/miR-31-5p/P2RX7/p38 MAPK axis in autoimmune inflammation, suggesting their potential as therapeutic targets for autoimmune dry eye.

Indexed as

AdenosineAutoimmune DiseasesDry Eye SyndromesMacrophagesMicroRNAsReceptors, Purinergic P2X7AnimalsFemaleHumansRabbitsSjogren's SyndromeAdenosineMicroRNAsMIRN31 microRNA, humanN-methyladenosineP2RX7 protein, humanReceptors, Purinergic P2X7m6Amacrophage polarizationmiR‐31‐5pp2x7 receptorsjogren's syndrome dry eye

Identifiers

PMID40068094
PMCPMC12061282

What Socratic holds

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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.