ReviewJournal of autoimmunity2018
Autophagy dysfunction in autoinflammatory diseases.
Review in Journal of autoimmunity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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
17 citing papers in PubMed, 27 citations in OpenAlex.
- Systemic metabolic, hormonal, and glycomic remodeling during a 72-hour fast in healthy adults: a pilot study.Croatian medical journal · 2026Article
- Lysosome-related proteins may have changes in the urinary exosomes of patients with acute gout attack.European journal of medical research · 2025Article
- Silencing aquaporin 1 inhibits autophagy to exert anti-rheumatoid arthritis effects in TNF-α-induced fibroblast-like synoviocytes and adjuvant-induced arthritis ratsInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Circ_0058051 Targeted miR-129-5P Regulates Autophagy-Related Gene ATG7 to Promote the Inflammation of Gout.Mediators of inflammation · 2025Article
- A systems immunology perspective on gout pathogenesis and its precision-targeted treatment strategies.Frontiers in immunology · 2025Review
- The haemagglutinin-neuraminidase protein of velogenic Newcastle disease virus enhances viral infection through NF-κB-mediated programmed cell death.Veterinary research · 2024Article
- Truncating NFKB1 variants cause combined NLRP3 inflammasome activation and type I interferon signaling and predispose to necrotizing fasciitis.Cell reports. Medicine · 2024Article
- Identifying functional dysregulation of NOD2 variant Q902K in patients with Yao syndrome.Arthritis research & therapy · 2024Article
- Race-specific association of an IRGM risk allele with cytokine expression in human subjects.Scientific reports · 2023Article
- Single-cell transcriptomic analysis in two patients with rare systemic autoinflammatory diseases treated with anti-TNF therapy.Frontiers in immunology · 2023Article
- NOD2 Versus MEFV: Differential Diagnosis of Yao Syndrome and Familial Mediterranean Fever.Rheumatology and immunology research · 2021Article
- An integrative multi-omics approach uncovers the regulatory role of CDK7 and CDK4 in autophagy activation induced by silica nanoparticles.Autophagy · 2021Article
- Oridonin suppresses autophagy and survival in rheumatoid arthritis fibroblast-like synoviocytes.Pharmaceutical biology · 2020Article
- Hypothesis: determining phenotypic specificity facilitates understanding of pathophysiology in rare genetic disorders.Journal of inherited metabolic disease · 2020Article
- Functional analysis of a novel G87V TNFRSF1A mutation in patients with TNF receptor-associated periodic syndrome.Clinical and experimental immunology · 2019Article
- Methylomic correlates of autophagy activity in cystic fibrosis.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2019Article
- The physiological roles of autophagy in the mammalian life cycle.Biological reviews of the Cambridge Philosophical Society · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Autoinflammatory diseases (AUIDs) are a genetically heterogeneous group of rheumatic diseases characterized by episodic inflammation linked with dysregulated innate immune responses. In this review, we summarize the molecular mechanisms altered by disease-associated variants in several AUIDs, including NOD2-associated diseases, TNF receptor-associated periodic syndrome (TRAPS), familial Mediterranean fever (FMF) and hyperimmunoglobulinemia D and periodic fever syndrome (HIDS), and highlight the roles dysregulated autophagy plays in disease pathogenesis. Autophagy is a conserved eukaryotic pathway for the elimination of cellular stressors, such as misfolded proteins, damaged organelles, or intracellular microorganisms. It is now recognized that autophagy also functions to control inflammation through regulatory interactions with innate immune signaling pathways. AUID-associated genetic variants are known to directly activate inflammatory signaling pathways. Recent evidence also indicates that these variants may also cause impairment of autophagy, thus augmenting inflammatory responses indirectly. Intriguingly, these variants can impair autophagy by different mechanisms, further implicating the autophagic response pathway in AUIDs. These discoveries provide evidence that autophagy could be investigated as a new therapeutic target for AUIDs.
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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.