Evidence map›Paper›PMID 32797249›Full record

ReviewInflammation research : official journal of the European Histamine Research Society ... [et al.]2020

Metabolic reprogramming as a key regulator in the pathogenesis of rheumatoid arthritis.

Wei-Wei Cai, Yun Yu, Shi-Ye Zong, Fang Wei

Abstract readReview
PubMed Publisher
In one paragraph

Review in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

39 citing papers in PubMed, 49 citations in OpenAlex.

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  20. Evaluation of the inhibitory mechanism ofFrontiers in pharmacology · 2024
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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

4 authors at 1 institution in 1 country.

Wei-Wei CaiSchool of Pharmacy, Bengbu Medical College, Bengbu, 233030, Anhui, China.
Yun YuSchool of Pharmacy, Bengbu Medical College, Bengbu, 233030, Anhui, China.
Shi-Ye ZongSchool of Pharmacy, Bengbu Medical College, Bengbu, 233030, Anhui, China.
Fang WeiSchool of Pharmacy, Bengbu Medical College, Bengbu, 233030, Anhui, China. weifangmailbox@126.com.ORCID http://orcid.org/0000-0002-8392-3243
Bengbu Medical College · CN

Funding

Anhui Province Postdoctoral Research Activity Funding Project 2018B251Innovative Drug Innovation Team of Bengbu Medical College BYKC201904National Natural Science Foundation of China 81703529the Innovation and Entrepreneurship Project Plan of National Undergraduate Support Project of China 201910367036
6 · The paper itself

Abstract

purposeRheumatoid arthritis (RA) is a chronic, systemic autoimmune disease with synovitis as pathological changes. The immune microenvironment of RA promotes metabolic reprogramming of immune cells and stromal cells, which leads to dysfunction and imbalance of immune homeostasis. Cell metabolism undergoes the switch from a static regulatory state to a highly metabolic active state, which changes the redox-sensitive signaling pathway and also leads to the accumulation of metabolic intermediates, which in turn can act as signaling molecules and further aggravate the inflammatory response. The reprogramming of immunometabolism affects the function of immune cells and is crucial to the pathogenesis of RA. In addition, mitochondrial dysfunction plays a key role in glycolytic reprogramming in RA. These metabolic changes may be potential therapeutic targets for RA. Therefore, we reviewed the metabolic reprogramming of RA immune cells and fibroblast-like synovium cells (FLS) and its relationship with mitochondrial dysfunction.

methodsA computer-based online search was performed using the PubMed database and Web of Science database for published articles concerning immunometabolic reprogramming, mitochondrial dysfunction, and rheumatoid arthritis.

resultsThis article reviews the metabolic reprogramming of immune cells and fibroblast-like synoviocytes in RA and their relationship to mitochondrial disfunction, as well as the key pro-inflammatory pathways associated with metabolic reprogramming and chemotherapy as a potential future therapeutic strategy for RA.

Indexed as

AnimalsArthritis, RheumatoidHumansMacrophagesMitochondriaSignal TransductionSynoviocytesT-LymphocytesFibroblast-like synoviocytesMacrophagesMetabolic reprogrammingMitochondrial dysfunctionRheumatoid arthritisT cells

Identifiers

PMID32797249
OpenAlexW3049193791

What OpenQuestion holds

Textmetadata
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.