Evidence map›Paper›PMID 37131409›Full record

ReviewJournal of inflammation research2023

The Involvement of Glucose and Lipid Metabolism Alteration in Rheumatoid Arthritis and Its Clinical Implication.

Ting-Ting Luo, Yi-Jin Wu, Qin Yin, Wen-Gang Chen, Jian Zuo

Open access · goldAbstract readReview
In one paragraph

Review in Journal of inflammation research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Frontier research on mechanisms of bone destruction in rheumatoid arthritis.Frontiers in cell and developmental biology · 2026
    Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Observational
  12. Administration of Liposomal-BasedInternational journal of nanomedicine · 2024
    Article
  13. 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

5 authors at 1 institution in 1 country.

Ting-Ting Luo *Department of Pharmacy, The Second Affiliated Hospital of Wannan Medical College, Wuhu, 241000, People's Republic of China.
Yi-Jin Wu *Department of Pharmacy, The Second Affiliated Hospital of Wannan Medical College, Wuhu, 241000, People's Republic of China.ORCID 0000-0002-6169-9084
Qin YinDepartment of Pharmacy, The Second Affiliated Hospital of Wannan Medical College, Wuhu, 241000, People's Republic of China.
Wen-Gang ChenDepartment of Pharmacy, The Second Affiliated Hospital of Wannan Medical College, Wuhu, 241000, People's Republic of China.
Jian ZuoXin'an Medical Research Center, The First Affiliated Hospital of Wannan Medical College, Wuhu, 241000, People's Republic of China.
Wannan Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obviously, immune cells like T cells and macrophages play a major role in rheumatoid arthritis (RA). On one hand, the breakdown of immune homeostasis directly induces systemic inflammation; on the other hand, these cells initiate and perpetuate synovitis and tissue damages through the interaction with fibroblast-like synoviocytes (FLS). In recent years, the pathological link between metabolic disorders and immune imbalance has received increasing attention. High energy demand of immune cells leads to the accumulation of metabolic byproducts and inflammatory mediators. They act on various metabolism-sensitive signal pathways as well as relevant transcription factors, such as HIF-1α, and STATs. These molecular events will impact RA-related effectors like circulating immune cells and joint-resident cells in return, allowing the continuous progression of systemic inflammation, arthritic manifestations, and life-threatening complications. In other words, metabolic complications are secondary pathological factors for the progression of RA. Therefore, the status of energy metabolism may be an important indicator to evaluate RA severity, and in-depth explorations of the mechanisms underlying the mystery of how RA-related metabolic disorders develop will provide useful clues to further clarify the etiology of RA, and inspire the discovery of new anti-rheumatic targets. This article reviews the latest research progress on the interactions between immune and metabolism systems in the context of RA. Great importance is attached to the changes in certain pathways controlling both immune and metabolism functions during RA progression.

Indexed as

immune cellsinflammationmetabolismrheumatoid arthritis

Identifiers

PMID37131409
PMCPMC10149064
OpenAlexW4367056204

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.