ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Bioinspired Claw-Engaged Adhesive Microparticles Armed with γGC Alleviate Ulcerative Colitis via Targeted Suppression of Macrophage Ferroptosis.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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Who cites it
7 citing papers in PubMed.
- Oral delivery of anti-mCD80 nanobody-engineered probiotic bacterial nanovesicles for macrophage-targeted Il17ra silencing in colitis.Journal of nanobiotechnology · 2026Article
- Monocyte-Derived Macrophage Ferroptosis Amplifies Cholangitis in Primary Biliary Cholangitis via a Calpain/ACSL4 Axis.Biomedicines · 2026Article
- Bioinformatic validation of LCN2 as a common hub gene for ferroptosis, pyroptosis and necroptosis in ulcerative colitis.BMC gastroenterology · 2026Article
- Identification and Validation of Ferroptosis-Related Biomarkers and Therapeutic Targets in ARDS: A Bioinformatics and Experimental Study.Journal of inflammation research · 2026Article
- Macrophage dysregulation in inflammatory bowel disease: cellular heterogeneity, pathogenic mechanism, and treatment.Frontiers in immunology · 2026Review
- Article
- Research progress of macrophage ferroptosis in inflammatory bowel disease and inflammation-cancer transformation.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
Ulcerative colitis (UC) is a chronic inflammatory bowel disease, characterized by focal iron overload. Herein, we reported that γ-glutamylcysteine (γGC) deletion in UC lesions intensified the disease by depleting intracellular GSH to induce macrophage ferroptosis, leading to macrophage M1 reprogramming and eventually exacerbating inflammation. To counteract this, the advanced microparticles (MPs)-based delivery system is selected to encapsulate γGC. The resulting γGC-MPs displayed the same porous and spiky morphology as their substrate's natural pollens, resulting in improved intestinal adhesion and enhanced lesion contact of γGC-MPs. Our results demonstrated that exogenous γGC supplementation could inhibit macrophage M1 polarization by restraining ferroptosis, as well as suppressing the PI3K/AKT pathway and TNF signaling pathway. Compared with free γGC, γGC-MPs significantly alleviated typical UC symptoms in dextran sulfate sodium (DSS)-induced colitis, evidenced by reduced intestinal inflammation, restored intestinal barrier function, and improved microbiota composition. Consequently, this study addressed critical gaps in understanding the causes of ferroptosis and its impact on macrophage reprogramming in UC, offering a novel synergistic therapeutic strategy for UC.
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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.