Evidence map›Paper›PMID 36213670›Full record

ReviewFrontiers in medicine2022

Rheumatoid arthritis and mitochondrial homeostasis: The crossroads of metabolism and immunity.

Liu Cui, Jing Weiyao, Su Chenghong, Liu Limei, Zhang Xinghua, Yuan Bo, Du Xiaozheng, Wang Haidong

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 2 pooled it
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

32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 45 citations in OpenAlex.

  1. Pooled it
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  9. A novel small molecule KMU-11361 attenuates rheumatoid arthritis by mechanistic inhibition of the TAK1-NF-κB-NLRP3 axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
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  11. Frontiers in veterinary science · 2026
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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

8 authors at 2 institutions in 1 country.

Liu CuiCollege of Acupuncture-Moxibustion and Tuina, Gansu University of Chinese Medicine, Lanzhou, China.
Jing WeiyaoCollege of Acupuncture-Moxibustion and Tuina, Gansu University of Chinese Medicine, Lanzhou, China.
Su ChenghongCollege of Acupuncture-Moxibustion and Tuina, Gansu University of Chinese Medicine, Lanzhou, China.
Liu LimeiCollege of Acupuncture-Moxibustion and Tuina, Gansu University of Chinese Medicine, Lanzhou, China.
Zhang XinghuaAcupuncture and Moxibustion Department, Gansu Provincial Hospital of Traditional Chinese Medicine (TCM), Lanzhou, China.
Yuan BoAcupuncture and Pain Department, Affiliated Hospital of Gansu University of Traditional Chinese Medicine (TCM), Lanzhou, China.
Du XiaozhengCollege of Acupuncture-Moxibustion and Tuina, Gansu University of Chinese Medicine, Lanzhou, China.
Wang HaidongRheumatoid Bone Disease Center, Gansu Provincial Hospital of Traditional Chinese Medicine (TCM), Lanzhou, China.
Gansu University of Traditional Chinese Medicine · CNGansu Provincial Hospital of TCM · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis is an autoimmune disease characterized by chronic symmetric synovial inflammation and erosive bone destruction. Mitochondria are the main site of cellular energy supply and play a key role in the process of energy metabolism. They possess certain self-regulatory and repair capabilities. Mitochondria maintain relative stability in number, morphology, and spatial structure through biological processes, such as biogenesis, fission, fusion, and autophagy, which are collectively called mitochondrial homeostasis. An imbalance in the mitochondrial homeostatic environment will affect immune cell energy metabolism, synovial cell proliferation, apoptosis, and inflammatory signaling. These biological processes are involved in the onset and development of rheumatoid arthritis. In this review, we found that in rheumatoid arthritis, abnormal mitochondrial homeostasis can mediate various immune cell metabolic disorders, and the reprogramming of immune cell metabolism is closely related to their inflammatory activation. In turn, mitochondrial damage and homeostatic imbalance can lead to mtDNA leakage and increased mtROS production. mtDNA and mtROS are active substances mediating multiple inflammatory pathways. Several rheumatoid arthritis therapeutic agents regulate mitochondrial homeostasis and repair mitochondrial damage. Therefore, modulation of mitochondrial homeostasis would be one of the most attractive targets for the treatment of rheumatoid arthritis.

Indexed as

apoptosis and proliferationenergy metabolismimmune cellsinflammatory pathwaysmitochondrial homeostasisrheumatoid arthritis

Identifiers

PMID36213670
PMCPMC9542797
OpenAlexW4297004472

What OpenQuestion 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 OpenQuestion graph.