Evidence map›Paper›PMID 41394899›Full record

ReviewJournal of inflammation research2025

The Role of Mitochondrial Regulation in Macrophage Polarization: Implications for the Pathogenesis of Rheumatoid Arthritis.

Pingshun Li, Gang Wang, Zhihui Peng, Lihuan Zhang, Fang Yang, Yong Wei, Meihan Pan, Haohao Zang, Mengru Zhou

Abstract readReview
In one paragraph

Review in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. 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

9 authors.

Pingshun LiDepartment of Rheumatology and Bone Disease, Affiliated Hospital of Gansu University of Chinese Medicine, Lanzhou, 730000, People's Republic of China.ORCID 0009-0001-9054-3249
Gang WangDepartment of Rheumatology and Bone Disease, Affiliated Hospital of Gansu University of Chinese Medicine, Lanzhou, 730000, People's Republic of China.
Zhihui PengSchool of Physical Education and Health, Gansu University of Chinese Medicine, Lanzhou, 730000, People's Republic of China.
Lihuan ZhangDepartment of Rheumatology and Bone Disease, Affiliated Hospital of Gansu University of Chinese Medicine, Lanzhou, 730000, People's Republic of China.
Fang YangDepartment of Rheumatology and Bone Disease, Affiliated Hospital of Gansu University of Chinese Medicine, Lanzhou, 730000, People's Republic of China.
Yong WeiDepartment of Rheumatology and Bone Disease, Affiliated Hospital of Gansu University of Chinese Medicine, Lanzhou, 730000, People's Republic of China.
Meihan PanCollege of Integrative Chinese and Western Medicine, Gansu University of Chinese Medicine, Lanzhou, 730000, People's Republic of China.
Haohao ZangCollege of Integrative Chinese and Western Medicine, Gansu University of Chinese Medicine, Lanzhou, 730000, People's Republic of China.
Mengru ZhouDepartment of Rheumatology and Bone Disease, Affiliated Hospital of Gansu University of Chinese Medicine, Lanzhou, 730000, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is an autoimmune arthropathy closely associated with chronic inflammation, whose pathogenesis involves macrophages, particularly M1 macrophage-induced inflammatory responses. Mitochondria, as key organelles governing macrophage metabolism and function, regulate M1/M2 macrophage polarization through multiple pathways and signaling molecules, thereby inducing immune and inflammatory responses that contribute to RA development. Therefore, this paper delves into the intricate mechanisms by which mitochondria regulate macrophage-specific polarization. These pathways encompass metabolic processes, signaling molecules, mitochondrial dynamics, mitochondrial-associated molecules, mitochondrial autophagy, ion homeostasis, and mitochondrial translocation. The study underscores the pivotal role of mitochondria in macrophage-specific polarization and highlights the potential for basic research to intervene in RA by modulating Mitochondrial metabolism, mitochondrial dynamics, mitochondrial autophagy, and mitochondrial translocation to promote M1-to-M2 macrophage conversion and suppress RA inflammatory responses. This holds significant implications for repairing RA-induced bone destruction and advancing clinical treatment.

Indexed as

inflammatory responseM1/M2 polarizationmacrophagespathogenesisrheumatoid arthritis

Identifiers

PMID41394899
PMCPMC12701075

What OpenQuestion holds

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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.