ReviewJournal of clinical medicine2020
Understanding the Complexity of Sjögren's Syndrome: Remarkable Progress in Elucidating NF-κB Mechanisms.
Review in Journal of clinical medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it.
- A meta-analysis of the effect of Sjögren's syndrome on adverse pregnancy outcomes.Clinics (Sao Paulo, Brazil) · 2022Pooled it
- Non-canonical NF-κB drives a fate switch from germinal center to early effector B cells.iScience · 2026Article
- Photobiomodulation for salivary gland dysfunction: aligning clinical expectations with etiology-dependent treatment responsiveness.Lasers in medical science · 2026Review
- NF‑κB signaling drives Th17‑mediated lacrimal gland injury and tear dysfunction in a murine model of primary Sjögren's syndrome.Molecular medicine reports · 2026Article
- Ectodysplasin-A (EDA) Signaling Cross-Talk in Skeletogenesis.Calcified tissue international · 2026Review
- Nitrate Prevents Sjögren's Disease by Modulating T Helper Cells via NF-κB Pathway Suppression.Oral diseases · 2025Article
- The antibody repertoire of autoimmune sensory neuronopathies targets pathways of the innate and adaptive immune system. An autoantigenomic approach.Journal of translational autoimmunity · 2025Article
- Significance of Notch Signaling in Salivary Gland Development and Diseases.Journal of clinical medicine · 2025Review
- Immune and non-immune mediators in the fibrosis pathogenesis of salivary gland in Sjögren's syndrome.Frontiers in immunology · 2024Review
- Relationship between Chinese Herbal Medicine Use and Risk of Sjögren's Syndrome in Patients with Rheumatoid Arthritis: A Retrospective, Population-Based, Nested Case-Control Study.Medicina (Kaunas, Lithuania) · 2023Article
- Salivary gland function, development, and regeneration.Physiological reviews · 2022Review
- Anti-Inflammatory Functions of Methanol Extract fromPlants (Basel, Switzerland) · 2022Article
- Sjögren's syndrome: a systemic autoimmune disease.Clinical and experimental medicine · 2022Review
- Association of the Risk of Primary Sjögren's Syndrome With Fibrocystic Breast Disease: A Nationwide, Population-Based Study.Frontiers in medicine · 2021Article
- Differentially Expressed Gene Pathways in the Conjunctiva of Sjögren Syndrome Keratoconjunctivitis Sicca.Frontiers in immunology · 2021Article
- Special Issue-"Diseases of the Salivary Glands".Journal of clinical medicine · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sjögren's syndrome (SS) is a systemic autoimmune inflammatory disease with a poorly defined aetiology, which targets exocrine glands (particularly salivary and lachrymal glands), affecting the secretory function. Patients suffering from SS exhibit persistent xerostomia and keratoconjunctivitis sicca. It is now widely acknowledged that a chronic grade of inflammation plays a central role in the initiation, progression, and development of SS. Consistent with its key role in organizing inflammatory responses, numerous recent studies have shown involvement of the transcription factor nuclear factor κ (kappa)-light-chain-enhancer of activated B cells (NF-κB) in the development of this disease. Therefore, chronic inflammation is considered as a critical factor in the disease aetiology, offering hope for the development of new drugs for treatment. The purpose of this review is to describe the current knowledge about the NF-κB-mediated molecular events implicated in the pathogenesis of SS.
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Registered trials
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.