Article in Arthritis & rheumatology (Hoboken, N.J.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing 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.
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
9 authors.
Gaurav SwarnkarWashington University School of Medicine, St. Louis, Missouri.
Musarrat NaazWashington University School of Medicine, St. Louis, Missouri.
Dorothy MimsWashington University School of Medicine, St. Louis, Missouri.
Prashant GuptaWashington University in St. Louis, Missouri.
Timothy PetersonWashington University School of Medicine, HealthSpan Technologies, Inc., and Bioio, Inc., St. Louis, Missouri.
Matthew J ChristopherWashington University School of Medicine, St. Louis, Missouri.
Srikanth SingamaneniWashington University in St. Louis, Missouri.
Gabriel MbalavieleWashington University School of Medicine, St. Louis, Missouri.ORCID 0000-0003-4660-0952
Yousef Abu-AmerWashington University School of Medicine and Shriners Hospital for Children, St. Louis, Missouri.ORCID 0000-0002-5890-5086
Funding
Resource Based Center for Musculoskeletal Biology and Medicine (Overall Application)P30AR074992 · NIAMS · WASHINGTON UNIVERSITY · PI MATTHEW J SILVA · 2019 to 2026
$6.8M
Differential Inflammasome Regulation in the pathogenesis of S. aureus osteomyelitisR01AI161022 · NIAID · WASHINGTON UNIVERSITY · PI CASSAT, JAMES E, MBALAVIELE, GABRIEL · 2021 to 2025
$3.4M
Molecular pathways of calcium pyrophosphate deposition diseaseR01AG077732 · NIA · MEDICAL COLLEGE OF WISCONSIN · PI Gabriel Mbalaviele, Ann K Rosenthal · 2022 to 2026
$2.4M
Development of Injectable Super-Lubricious Microgels for Sustained Release of Platelet-Rich Plasma to Treat Post-Traumatic OsteoarthritisR01AR081270 · NIAMS · SAINT LOUIS UNIVERSITY · PI Yousef Abu-Amer, Silviya Petrova Zustiak · 2023 to 2026
$2.1M
Regulation of Osteoclastogenesis and Inflammatory OsteolysisR01AR082192 · NIAMS · WASHINGTON UNIVERSITY · PI Yousef Abu-Amer · 2023 to 2026
$1.9M
Role of gasdermin D in bone resorptionR01AR076758 · NIAMS · WASHINGTON UNIVERSITY · PI MBALAVIELE, GABRIEL · 2020 to 2024
$1.9M
Novel insulin-sensitizing NASH/diabetes drugs.R42DK121652 · NIDDK · BIOIO, LLC · PI FINCK, BRIAN N, PETERSON, TIMOTHY R · 2019 to 2022
$1.7M
Mechanisms of Physiologic and Pathologic OsteoclastogenesisR01AR072623 · NIAMS · WASHINGTON UNIVERSITY · PI ABU-AMER, YOUSEF · 2018 to 2022
$1.7M
Cabinet microCT System for Musculoskeletal Specimen ImagingS10OD028573 · OD · WASHINGTON UNIVERSITY · PI SILVA, MATTHEW J · 2020 to 2020
$407k
Drug target identification using CRISPRi/a screeningR41GM137625 · NIGMS · BIOIO, LLC · PI GILBERT, LUKE, PETERSON, TIMOTHY R · 2020 to 2020
$224k
NIAID NIH HHS R01 AI161022NIAMS NIH HHS P30 AR074992NIAMS NIH HHS R01 AR072623NIAMS NIH HHS R01 AR076758NIAMS NIH HHS R01 AR081270NIAMS NIH HHS R01 AR082192NIA NIH HHS R01 AG077732NIDDK NIH HHS R42 DK121652NIGMS NIH HHS R41 GM137625NIH and National Institute of Arthritis and Musculoskeletal and Skin Diseases R01-AG077732NIH and National Institute of Arthritis and Musculoskeletal and Skin Diseases R01-AI161022NIH and National Institute of Arthritis and Musculoskeletal and Skin Diseases R01-AR072623NIH and National Institute of Arthritis and Musculoskeletal and Skin Diseases R01-AR076758NIH and National Institute of Arthritis and Musculoskeletal and Skin Diseases R01-AR081270NIH and National Institute of Arthritis and Musculoskeletal and Skin Diseases R01-AR082192NIH Core Center for Musculoskeletal Biology and Medicine P30-AR074992NIH HHS S10 OD028573Shriners Hospital for Children 85109
6 · The paper itself
Abstract
objectiveCurrent therapies targeting individual factors in inflammatory arthritis show variable efficacy, often requiring treatment with combinations of drugs, and are associated with undesirable side effects. NF-ĸB is critical for the production and function of most inflammatory cytokines. However, given its essential role in physiologic processes, targeting NF-ĸB is precarious. Hence, identifying pathways downstream of NF-ĸB that selectively govern the expression of inflammatory cytokines in inflammatory arthritis would be advantageous. We have previously identified IĸBζ as a unique inflammatory signature of NF-ĸB that controls the transcription of inflammatory cytokines only under pathologic conditions while sparing physiologic NF-ĸB signals.
methodsWe generated mice harboring myeloid, lymphoid, and global deletion of Nfkbiz (the gene encoding IĸBζ). These models were subjected to serum transfer-induced arthritis. Additionally, pharmacologic inhibitors of IĸBζ were injected intraperitonially. Joint swelling, microcomputed tomography, immunohistochemistry, flow cytometry, and cytokine measurements were conducted using synovial tissue samples.
resultsGlobal deletion of Nfkbiz or depletion of neutrophils (vastly IĸBζ
conclusionOur study positions IĸBζ as an inflammation-specific target for therapeutic consideration in rheumatoid arthritis because its inhibition spares the beneficial functions of NF-ĸB.
Indexed as
Arthritis, ExperimentalI-kappa B KinaseNF-kappa BAdaptor Proteins, Signal TransducingAnimalsCytokinesDisease Models, AnimalMiceSynovial MembraneX-Ray MicrotomographyAdaptor Proteins, Signal TransducingCytokinesI-kappa B KinaseNF-kappa BNfkbiz protein, mouse
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.
IĸBζ as a Central Modulator of Inflammatory Arthritis Pathogenesis. · full record | OpenQuestion