ReviewInternational journal of molecular sciences2026
Exosome-Mediated Intercellular Communication in the Pathological Processes of Gouty Arthritis and Its Treatment.
Review in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Neutrophil Fate and Function in Gout: From Sterile Inflammation to Resolution.International journal of molecular sciences · 2026Review
- Astragaloside IV and rapamycin co-loaded bone marrow mesenchymal stem cell-derived exosome nanocarriers for targeted modulation of the PI3K/Akt/mTOR pathway in hepatocellular carcinoma.Nanomedicine (London, England) · 2026Article
- The Dual Role of Exosomes in Gout: From Inflammatory Amplifiers to Therapeutic Regulators.Inflammation · 2026Review
- A Novel Dual URAT1/GLUT9 Inhibitor Reduces Hyperuricemia by Enhancing Uric Acid Excretion and Attenuating Renal Fibrosis.Pharmaceuticals (Basel, Switzerland) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Gouty arthritis (GA) is a debilitating autoinflammatory disorder precipitated by the deposition of monosodium urate (MSU) crystals, leading to intense, recurrent joint inflammation and systemic metabolic dysregulation. While hyperuricemia is a prerequisite, the transition to clinical gout involves complex intercellular signaling cascades that are not fully understood. Emerging evidence has identified exosomes,- nanoscale extracellular vesicles, -as critical mediators in this pathological process. Exosomes function as intercellular carriers, transporting a diverse cargo of bioactive molecules, including proteins, lipids, and nucleic acids (e.g., microRNAs), which profoundly influence immune cell activation, inflammasome regulation, and metabolic pathways. This review provides a critical analysis of the dual role of exosomes in both propagating and potentially resolving inflammation in GA. We delve into the intricate mechanisms of exosome-mediated pathogenesis, including the modulation of purine metabolism, lysosomal function, and complement-inflammasome crosstalk. Furthermore, we explore the burgeoning field of exosome-based therapeutics, critically evaluating strategies such as engineered exosomes for targeted drug delivery, mesenchymal stem cell (MSC)-derived exosomes for immunomodulation, and the development of exosomal biomarkers for diagnostics. Additionally, we examine how chemical drugs and herbal compounds may exert therapeutic effects by modulating exosome pathways, offering new insights into integrative treatment approaches. By synthesizing recent findings from proteomic, transcriptomic, and functional studies, we aim to unravel the complexities of exosome signaling in GA and to propose innovative therapeutic avenues that target these pathways to improve patient outcomes.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.