Evidence map›Paper›PMID 36845127›Full record

ReviewFrontiers in immunology2023

Role of reactive oxygen species and mitochondrial damage in rheumatoid arthritis and targeted drugs.

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

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
25.9field-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

62 citing papers in PubMed, 104 citations in OpenAlex.

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  15. Nanozyme-based therapies for inflammatory immune disorders: opportunities and challenges.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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2 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

10 authors at 2 institutions in 1 country.

Weiyao JingDepartment of Acupuncture-Moxibustion and Tuina, Gansu University of Chinese Medicine, Lanzhou, China.
Cui LiuDepartment of Acupuncture-Moxibustion and Tuina, Gansu University of Chinese Medicine, Lanzhou, China.
Chenghong SuDepartment of Acupuncture-Moxibustion and Tuina, Gansu University of Chinese Medicine, Lanzhou, China.
Limei LiuDepartment of Acupuncture-Moxibustion and Tuina, Gansu University of Chinese Medicine, Lanzhou, China.
Ping ChenDepartment of Rheumatic and Bone Disease, Gansu Provincial Hospital of Traditional Chinese Medicine, Lanzhou, China.
Xiangjun LiDepartment of Rheumatic and Bone Disease, Gansu Provincial Hospital of Traditional Chinese Medicine, Lanzhou, China.
Xinghua ZhangDepartment of Acupuncture, Gansu Provincial Hospital of Traditional Chinese Medicine, Lanzhou, China.
Bo YuanDepartment of Acupuncture and Pain, Affiliated Hospital of Gansu University of Traditional Chinese Medicine, Lanzhou, China.
Haidong WangDepartment of Rheumatic and Bone Disease, Gansu Provincial Hospital of Traditional Chinese Medicine, Lanzhou, China.
Xiaozheng DuDepartment of Acupuncture-Moxibustion and Tuina, Gansu University of Chinese Medicine, Lanzhou, China.
Gansu University of Traditional Chinese Medicine · CNGansu Provincial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rheumatoid arthritis (RA) is an autoimmune disease characterized by synovial inflammation, pannus formation, and bone and cartilage damage. It has a high disability rate. The hypoxic microenvironment of RA joints can cause reactive oxygen species (ROS) accumulation and mitochondrial damage, which not only affect the metabolic processes of immune cells and pathological changes in fibroblastic synovial cells but also upregulate the expression of several inflammatory pathways, ultimately promoting inflammation. Additionally, ROS and mitochondrial damage are involved in angiogenesis and bone destruction, thereby accelerating RA progression. In this review, we highlighted the effects of ROS accumulation and mitochondrial damage on inflammatory response, angiogenesis, bone and cartilage damage in RA. Additionally, we summarized therapies that target ROS or mitochondria to relieve RA symptoms and discuss the gaps in research and existing controversies, hoping to provide new ideas for research in this area and insights for targeted drug development in RA.

Indexed as

Arthritis, RheumatoidSynovial MembraneBone and BonesHumansInflammationReactive Oxygen SpeciesReactive Oxygen Speciesmitochondrial damageoxidative stressreactive oxygen speciesrheumatoid arthritistargeted drugs

Identifiers

PMID36845127
PMCPMC9948260
OpenAlexW4319744529

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.