ArticleInternational journal of biological sciences2024
IL-33 Accelerates Chronic Atrophic Gastritis through AMPK-ULK1 Axis Mediated Autolysosomal Degradation of GKN1.
Article in International journal of biological sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- Alkaloids Mediate Multi-Level Modulation of Gastric Carcinogenesis: From Antibacterial and Anti-Inflammatory Actions to Antitumor Effects.International journal of molecular sciences · 2026Review
- 5-Hydroxymethylfurfural and Isoverbascoside Alleviate Oxidative Damage INS-1 and MIN6 β-Cells by Activating Autophagy and Inhibiting Apoptosis.Metabolites · 2026Article
- Integrated Multiomics Analysis Reveals Manual Therapy Restores Autophagic Homeostasis via the AMPK/ULK1 Axis in Chronic Low Back Pain.Pain research & management · 2026Article
- Integrating network analysis and experimental validation to reveal the ferroptosis-associated mechanism of velvet antler in the treatment of chronic atrophic gastritis.Journal of food and drug analysis · 2025Article
- Weifuchun alleviates MNNG-induced chronic atrophic gastritis by improving the gastric and intestinal microbiota homeostasis.PloS one · 2025Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic atrophic gastritis (CAG) is a complex disease characterized by atrophy and inflammation in gastric mucosal tissue, especially with high expression of interleukins. However, the interaction and mechanisms between interleukins and gastric mucosal epithelial cells in CAG remain largely elusive. Here, we elucidate that IL-33 stands out as the predominant inflammatory factor in CAG, and its expression is induced by
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Registered trials
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