ArticleChinese medicine2025
Electroacupuncture attenuates intestinal epithelial ferroptosis in inflammatory bowel disease via Piezo1-mediated mitochondrial homeostasis.
Article in Chinese medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Piezo1 in digestive homeostasis and disease: Barrier function, immune signalling, cellular injury and metabolism.Clinical and translational medicine · 2026Review
- Sympathetic Overactivation Drives Neurogenic Alveolar Epithelial Pyroptosis via the PIEZO2-ER Stress Pathway in Acute Lung Injury Following Intracerebral Hemorrhage.CNS neuroscience & therapeutics · 2026Article
- Dynamin-Related Protein 1 (Drp1) in Inflammatory Bowel Disease: Molecular Pathways Connecting Mitochondrial Dynamics with Intestinal Inflammation and Homeostasis.International journal of molecular sciences · 2026Review
- Canonical pathways and selective mechanisms of autophagy in inflammatory bowel disease.Advanced biotechnology · 2026Review
- Evaluation of electroacupuncture acupoint selection's potential in the treatment of inflammatory bowel disease: an investigation using a mouse gut microbiome and metabolomics model.Frontiers in cellular and infection microbiology · 2026Article
- Acupoint Catgut Embedding Ameliorates Ulcerative Colitis in Association with Modulation of cGAS-STING Signaling and M1-Like/M2-Like Macrophage Markers.Journal of inflammation research · 2026Article
- Probiotics for ulcerative colitis: mechanisms, therapeutic advances, and emerging strategies.Frontiers in microbiology · 2026Review
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Authors and funding
6 authors.
Funding
Abstract
backgroundInflammatory bowel disease (IBD) involves pathological mechanical forces transduced by mechanosensitive Piezo1 channels. While electroacupuncture (EA) alleviates IBD injury, its relationship with Piezo1-mediated ferroptosis remains unknown.
methodsDextran sulfate sodium (DSS)-induced IBD mice and mechanically stressed HIEC-6 intestinal epithelial cells received EA or pharmacological modulators. Pathological scoring, transmission electron microscopy (TEM), inflammatory cytokine assays, Western blotting, and immunofluorescence evaluated mitochondrial dynamics and ferroptosis markers to elucidate the Piezo1-ferroptosis axis and EA's regulatory role.
resultsEA significantly reduced disease activity index (DAI), histopathological scores, colon shortening, and pro-inflammatory cytokines in IBD mice. By inhibiting fission, indicated by a decrease in dynamin-related protein 1 (DRP1), and mitophagy, shown by a reduction in Parkinson protein 2 (PARK2), EA maintained mitochondrial homeostasis. This effect was similar to ferroptosis inhibitor ferrostatin-1 (Fer-1). Moreover, EA lessened RSL3-induced exacerbation of ferroptosis. In vitro, mechanical stress or the Piezo1 agonist Yoda1 induced ferroptosis, which was evident from increased acyl-CoA synthetase Long-chain family member 4 (ACSL4), reactive oxygen species (ROS), malondialdehyde (MDA) and Fe
conclusionPiezo1-mediated mitochondrial dyshomeostasis critically drives intestinal epithelial ferroptosis in IBD. EA regulates Piezo1 to maintain mitochondrial homeostasis and suppresses ferroptosis, offering a potential therapeutic strategy for IBD.
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