ReviewDrug design, development and therapy2026
Artemisinin-Related Therapeutic Strategies for Autoimmune Thyroiditis: Chemokine-Receptor Networks, Spatial Thyroid Biology, and Molecular Mechanisms.
Review in Drug design, development and therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autoimmune thyroiditis (AIT) is a chronic immune-mediated thyroid disorder characterized by lymphocytic infiltration, follicular epithelial injury, autoantibody production, and variable progression to thyroid dysfunction. Because current management is largely supportive or replacement based, there is growing interest in interventions that might modify inflammatory and immune processes before irreversible tissue damage develops. This narrative review critically evaluates the potential, but not yet established, role of Artemisia-derived and artemisinin-related compounds in AIT. The analysis focuses on chemokine-receptor networks, spatial organization of thyroid inflammation, and molecular mechanisms linking endoperoxide/redox chemistry, innate immune signaling, and immune-cell trafficking. Evidence was identified through targeted, non-systematic searches of PubMed and Google Scholar, supported by backward and forward citation tracking. Thyroid-specific evidence remains limited and predominantly preclinical. Dihydroartemisinin (DHA) has been reported to attenuate experimental autoimmune thyroiditis by reducing inflammatory infiltration, thyroid autoantibodies, Th1/Th17-associated responses, CXCL10/CXCR3-linked signaling, and oxidative stress. Evidence from non-thyroid autoimmune and inflammatory models suggests additional effects on NF-κB, MAPK, PI3K/Akt/mTOR, JAK/STAT, TLR/MyD88, NRF2/GPX4-related redox responses, inflammasome activity, regulatory T-cell balance, and possible epigenetic remodeling; however, these findings should be treated as mechanistic context rather than direct evidence for human AIT. Most available studies involve purified or semi-synthetic compounds rather than standardized botanical preparations, and robust clinical validation is absent. Artemisinin-related compounds are therefore framed as hypothesis-driven immunomodulatory candidates that require thyroid-specific replication, target validation, comparative pharmacology, safety assessment, formulation standardization, and carefully designed translational studies before clinical application can be considered.
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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.