ReviewInflammation2026
Autophagy in Rheumatoid Arthritis: Molecular Mechanisms, Diagnostic Biomarkers, and Emerging Therapeutic Strategies.
Review in Inflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Targeting mitochondrial fission-autophagy axis in rheumatoid arthritis: leflunomide promote apoptosis of fibroblast-like synoviocytes.Arthritis research & therapy · 2026Article
- Endoplasmic Reticulum Stress as a Stage-Dependent Regulatory Hub in Rheumatoid Arthritis.Journal of inflammation research · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rheumatoid arthritis (RA) is a chronic autoimmune disorder marked by persistent synovial inflammation, joint destruction, and systemic complications. Recent research has revealed the complex involvement of autophagy, a cellular degradation and recycling process, in the pathogenesis and progression of RA. This review provides a comprehensive analysis of autophagy's multifaceted roles across immune regulation, synovial hyperplasia, osteoclastogenesis, and antigen presentation. Particular attention is given to the dualistic nature of autophagy, which may exert both protective and pathogenic effects depending on the cellular context and disease stage. We explore key molecular pathways regulating autophagy, including the mTOR, AMPK, and ULK1 axes, and detail how these are modulated by cytokines and signaling molecules characteristic of the RA inflammatory milieu. Epigenetic and genetic factors, including polymorphisms in ATG and BECN1 genes, microRNA regulation, and histone modifications, are also examined for their impact on autophagic flux and immune dysregulation. The diagnostic potential of autophagy-related biomarkers is discussed through transcriptomic and bioinformatics studies that stratify RA subtypes and correlate autophagic activity with disease severity. Additionally, we review therapeutic strategies targeting autophagy, encompassing conventional DMARDs, biologics, small molecules, nanoparticles, and phytochemicals. While modulating autophagy shows clinical promise, challenges remain regarding safety, specificity, and long-term efficacy. The integration of high-throughput omics technologies with artificial intelligence presents new opportunities to refine diagnostic precision and develop personalized therapeutic interventions. This review underscores the necessity of further translational research to define context-specific roles of autophagy in RA and to harness its potential in advancing precision medicine.
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What Socratic holds
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 Socratic graph.