ArticleChinese medicine2026
Targeting the ferritinophagy axis: multi-target regulation of TFRC/FTH1/NCOA4 by artesunate ameliorates salivary gland dysfunction in Sjögren's Disease.
Article in Chinese medicine, 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
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Who cites it
2 citing papers in PubMed.
- Artesunate in Ferroptosis and Cuproptosis Regulation: Context-Dependent Mechanisms, Interplay, and Therapeutic Implications.International journal of molecular sciences · 2026Review
- Review
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Authors and funding
8 authors.
Funding
Abstract
backgroundSjögren's Disease (SJD) is an autoimmune disorder involving lymphocytic infiltration of exocrine glands, notably salivary and lacrimal glands, causing dysfunction. Ferroptosis, an iron-dependent cell death pathway, contributes to glandular injury. Ferritinophagy, regulated by the TFRC/FTH1/NCOA4 axis, releases iron and promotes ferroptosis. Effective therapeutic strategies targeting this axis are limited.
objectiveTo investigate if artesunate (ART), an artemisinin derivative with anti-inflammatory/antioxidant properties, inhibits ferroptosis by modulating the TFRC/FTH1/NCOA4 axis and alleviates salivary gland dysfunction in SJD.
methodsNon-Obese Diabetic (NOD) mice (SJD model) were orally treated with ART. IFN-γ induced ferroptosis in human salivary gland (A253) cells. Analyses included scRNA-seq, bulk RNA-seq, molecular docking, Western blotting, immunofluorescence, flow cytometry, and functional assays.
resultsART significantly improved salivary gland histopathology and function in NOD mice, reducing inflammatory infiltration and increasing saliva flow. ART also lowered serum IgG and hepatic/renal dysfunction markers. Cellularly, ART suppressed IFN-γ-induced lipid peroxidation, mitochondrial damage, and rescued viability and aquaporin 5 (AQP5) expression. Mechanistically, ART modulated the TFRC/FTH1/NCOA4 axis: downregulating TFRC (iron uptake), upregulating FTH1 (iron storage), and reducing NCOA4 and LC3-II/I (suppressing ferritinophagy), ultimately downregulating heme iron levels. Docking indicated that ART binds the FTH1-NCOA4 interface, potentially hindering ferritin degradation. ART also upregulates GPX4 and xCT, synergistically inhibiting ferroptosis.
conclusionART mitigates SJD-associated salivary gland dysfunction by dually targeting the ferritinophagy axis (TFRC/FTH1/NCOA4 modulation) and augmenting antioxidant defense, supporting novel therapeutics targeting ferroptosis for SJD.
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