Evidence map›Paper›PMID 37332618›Full record

ReviewMediators of inflammation2023

Regulatory Mechanism of M1/M2 Macrophage Polarization in the Development of Autoimmune Diseases.

Yuan Peng, Mengxian Zhou, Hong Yang, Ruyi Qu, Yan Qiu, Jiawen Hao, Hongsheng Bi, Dadong Guo

Open access · goldAbstract readReview
In one paragraph

Review in Mediators of inflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
127citing papers in PubMed, 2 pooled it
25.0field-weighted citation impact, top 1% 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

127 citing papers in PubMed, 2 syntheses or guidelines pooled it, 152 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. The M1/M2 Test System for Determining Macrophage Phenotypes.International journal of molecular sciences · 2026
    Review
  10. Ion-Driven Regulation of CaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Liver Macrophages in the Pathogenesis of Viral Hepatitis.Current issues in molecular biology · 2026
    Review
  19. Review
  20. Article

67 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

8 authors at 1 institution in 1 country.

Yuan PengShandong University of Traditional Chinese Medicine, Jinan 250002, China.ORCID https://orcid.org/0000-0002-4133-8329
Mengxian ZhouShandong University of Traditional Chinese Medicine, Jinan 250002, China.ORCID https://orcid.org/0000-0002-4343-869X
Hong YangQingdao Traditional Chinese Medicine Hospital (Qingdao Hiser Hospital), Qingdao 266033, China.ORCID https://orcid.org/0009-0001-8683-4633
Ruyi QuShandong University of Traditional Chinese Medicine, Jinan 250002, China.ORCID https://orcid.org/0000-0003-1842-3063
Yan QiuThe Second Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan 250002, China.ORCID https://orcid.org/0000-0002-9145-6278
Jiawen HaoShandong University of Traditional Chinese Medicine, Jinan 250002, China.ORCID https://orcid.org/0000-0002-7242-9661
Hongsheng BiShandong Provincial Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Therapy of Ocular Diseases; Shandong Academy of Eye Disease Prevention and Therapy, Medical College of Optometry and Ophthalmology, Shandong University of Traditional Chinese Medicine, Jinan 250002, China.ORCID https://orcid.org/0000-0002-6965-9626
Dadong GuoShandong Provincial Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Therapy of Ocular Diseases; Shandong Academy of Eye Disease Prevention and Therapy, Medical College of Optometry and Ophthalmology, Shandong University of Traditional Chinese Medicine, Jinan 250002, China.ORCID https://orcid.org/0000-0002-1712-0055
Shandong University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages are innate immune cells in the organism and can be found in almost tissues and organs. They are highly plastic and heterogeneous cells and can participate in the immune response, thereby playing a crucial role in maintaining the immune homeostasis of the body. It is well known that undifferentiated macrophages can polarize into classically activated macrophages (M1 macrophages) and alternatively activated macrophages (M2 macrophages) under different microenvironmental conditions. The directions of macrophage polarization can be regulated by a series of factors, including interferon, lipopolysaccharide, interleukin, and noncoding RNAs. To elucidate the role of macrophages in various autoimmune diseases, we searched the literature on macrophages with the PubMed database. Search terms are as follows: macrophages, polarization, signaling pathways, noncoding RNA, inflammation, autoimmune diseases, systemic lupus erythematosus, rheumatoid arthritis, lupus nephritis, Sjogren's syndrome, Guillain-Barré syndrome, and multiple sclerosis. In the present study, we summarize the role of macrophage polarization in common autoimmune diseases. In addition, we also summarize the features and recent advances with a particular focus on the immunotherapeutic potential of macrophage polarization in autoimmune diseases and the potentially effective therapeutic targets.

Indexed as

Arthritis, RheumatoidLupus Erythematosus, SystemicLupus NephritisHumansInflammationMacrophage ActivationMacrophages

Identifiers

PMID37332618
PMCPMC10270764
OpenAlexW4379877729

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.