Evidence map›Paper›PMID 39550308›Full record

ReviewSeminars in arthritis and rheumatism2025

Metabolic checkpoints in rheumatoid arthritis.

Cornelia M Weyand, Jörg J Goronzy

Abstract readReview
In one paragraph

Review in Seminars in arthritis and rheumatism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed.

  1. Review
  2. Review
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  4. Immune responses in aging adults.The Journal of clinical investigation · 2026
    Review
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  10. Review
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  18. Review
  19. Article
  20. Glycosylation Regulation by TMEM230 in Aging and Autoimmunity.International journal of molecular sciences · 2025
    Article
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

2 authors.

Cornelia M WeyandDepartment of Medicine, Mayo Clinic Alix School of Medicine, Rochester, MN, 55905, USA; Department of Immunology, Mayo Clinic College of Medicine and Science, Rochester, MN, 55905, USA; Department of Cardiovascular Medicine, Mayo Clinic Alix School of Medicine, Rochester, MN, USA; Department of Medicine, Stanford University School of Medicine, Stanford, CA, 94305, USA. Electronic address: cweyand@stanford.edu.
Jörg J GoronzyDepartment of Medicine, Mayo Clinic Alix School of Medicine, Rochester, MN, 55905, USA; Department of Immunology, Mayo Clinic College of Medicine and Science, Rochester, MN, 55905, USA; Department of Medicine, Stanford University School of Medicine, Stanford, CA, 94305, USA.

Funding

VACCINE INDUCED IMMUNITY IN THE YOUNG AND AGEDU19AI057266 · NIAID · EMORY UNIVERSITY · PI Rafi Ahmed · 2003 to 2026
$81.7M
The NOTCH Signaling Pathway in Large Vessel VasculitisR01HL117913 · NHLBI · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 2014 to 2025
$5.0M
Oligoclonal T Cell Expansion &Rheumatoid ArthritisR01AR042527 · NIAMS · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 1993 to 2022
$4.8M
microRNA Regulation of T Cell SenescenceR01AI108891 · NIAID · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI GORONZY, JORG J · 2014 to 2023
$4.6M
Telomere Damage Responses and Immune AgingR01AI108906 · NIAID · STANFORD UNIVERSITY · PI WEYAND, CORNELIA M. · 2014 to 2024
$4.0M
Influence of Age on CD4 T Memory CellsR01AG045779 · NIA · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI GORONZY, JORG J · 2013 to 2023
$4.0M
T Cell Immunity in Giant Cell ArteritisR01HL142068 · NHLBI · STANFORD UNIVERSITY · PI Cornelia M. Weyand · 2018 to 2026
$3.3M
Memory T Cell Development and Survival in T Cell Responses of Older IndividualsR01AI129191 · NIAID · PALO ALTO VETERANS INSTIT FOR RESEARCH · PI GORONZY, JORG J · 2017 to 2021
$1.9M
Mechanisms of genetic variants in TH2 autoimmunityR01AI184360 · NIAID · MAYO CLINIC ROCHESTER · PI JORG J GORONZY · 2024 to 2026
$1.8M
Mitochondrial Malfunction in T Cell Aging and Tissue InflammationU01AI179609 · NIAID · MAYO CLINIC ROCHESTER · PI Cornelia M. Weyand · 2024 to 2026
$1.7M
NHLBI NIH HHS R01 HL117913NHLBI NIH HHS R01 HL142068NIAID NIH HHS R01 AI108891NIAID NIH HHS R01 AI108906NIAID NIH HHS R01 AI129191NIAID NIH HHS R01 AI184360NIAID NIH HHS U01 AI179609NIAID NIH HHS U19 AI057266NIAMS NIH HHS R01 AR042527NIA NIH HHS R01 AG045779
6 · The paper itself

Abstract

backgroundRheumatoid Arthritis is a systemic autoimmune disease affecting 0.5-1 % of the population. Despite a growing therapeutic armamentarium, RA remains incurable, and many patients suffer significant morbidity over time. The strongest genetic risk derives from HLA class II polymorphisms, implicating T cells as pathogenic drivers. Innate immune cells, e.g. monocytes and macrophages (Mⱷ) contribute to chronic tissue inflammation through an array of pro-inflammatory functions but also present antigen to autoreactive T cells. Differentiation, survival, and effector functions of both T cells and Mⱷ are ultimately controlled by their bioenergetic and biosynthetic programs, identifying cellular metabolism as a critical disease mechanism in RA.

objectivesSummarize current knowledge about metabolic conditions in the RA joint and disease-relevant metabolic circuits shaping the effector repertoire of RA T cells and Mⱷ.

resultsThe rheumatoid joint is a glucose deplete tissue environment, selecting for invading immune cells that can survive on non-glucose fuel sources. Inflamed synovium instead offers the amino acid glutamine and RA CD4

Indexed as

Arthritis, RheumatoidT-LymphocytesEnergy MetabolismHumansMacrophagesMitochondriaAcetyl-CoAAspartateATPCathepsinCitrateCytokinesGlycolysisMacrophagesMitochondriaRFX5T cellsTNF

Identifiers

PMID39550308
PMCPMC11761375

What OpenQuestion holds

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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.