ReviewMolecular biology reports2026
Exosome in Hashimoto's thyroiditis: from pathogenesis to diagnostic and therapeutic potential.
Review in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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
0 citing papers in PubMed.
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hashimoto's thyroiditis (HT), the most prevalent autoimmune thyroid disorder, arises from a complex interplay of genetic susceptibility, environmental triggers, and immune dysregulation. Emerging evidence highlights exosomes-small extracellular vesicles measuring 30-150 nm-as key mediators of intercellular communication and immune modulation in autoimmune disease. In HT, exosomal HSP60 released from IFN‑γ-stimulated thyroid follicular cells acts as an autoantigen cross‑reacting with TPO and TG, promoting thyrocyte injury through antigen-antibody interactions. T‑cell-derived exosomes enriched in miR‑142‑3p impair regulatory T‑cell function and exacerbate thyrocyte destruction by suppressing RAC1 and inhibiting ERK1/2 signaling. Patient‑derived exosomes containing elevated TPO and MHC‑II activate dendritic cells via TLR2/3 and NF‑κB pathways, driving Th1/Th17 polarization while suppressing Treg differentiation. Proteomic studies further reveal distinct exosomal signatures in HT, including increased immunomodulatory proteins such as HGFL, FAK1, and PTN12. Therapeutically, inhibition of exosome release (e.g., GW4869) and the use of engineered mesenchymal stem cell-derived exosomes demonstrate promising potential for restoring immune homeostasis. Collectively, these findings position exosomes as central contributors to HT pathogenesis and highlight their value as emerging diagnostic biomarkers and targets for innovative immunotherapeutic strategies.
Indexed as
Identifiers
42631765What 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.