ArticleThe Journal of clinical investigation2019
Endogenous glucocorticoids prevent gastric metaplasia by suppressing spontaneous inflammation.
Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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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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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
37 citing papers in PubMed, 55 citations in OpenAlex.
- The origins and progression of pyloric metaplasia following gastric mucosal injury.Physiological reviews · 2026Review
- Stomach at the crossroads: nuclear receptor signaling at the interface between what we are and what we eat.Physiological reviews · 2026Review
- Targeting the Correa's cascade of gastric cancer: the potential role of phytochemicals and autophagy modulation.Frontiers in pharmacology · 2026Review
- Role of circulating tumor DNA methylation in gastric cancer initiation and progression: A comprehensive review.World journal of gastrointestinal oncology · 2025Review
- Article
- Traditional Chinese medicine for chronic atrophic gastritis: Efficacy, mechanisms and targets.World journal of gastroenterology · 2025Review
- Mechanistic Insights into the Therapeutic Potential of Phytochemicals Against Stress-Induced Gastric Ulcer.Journal of inflammation research · 2025Review
- Emerging role of spasmolytic polypeptide-expressing metaplasia in gastric cancer.Journal of gastrointestinal oncology · 2024Review
- Immune-enhancing effects of endogenous glucocorticoids on gastric macrophages contribute to the development of gastric inflammation and metaplasia.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Endogenous glucocorticoids are required for normal macrophage activation and gastricAmerican journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Glucocorticoid Receptor Signaling Is Critical for Mouse Corneal Development, Inhibition of Inflammatory Response, and Neovascularization of the Cornea.The American journal of pathology · 2024Article
- Gastric Cancer and Intestinal Metaplasia: Differential Metabolic Landscapes and New Pathways to Diagnosis.International journal of molecular sciences · 2024Article
- Identification of collagen subtypes of gastric cancer for distinguishing patient prognosis and therapeutic response.Cancer innovation · 2024Article
- Comparison of gastric inflammation and metaplasia induced byMicrobiology spectrum · 2024Article
- Immune Cell Migration to Cancer.Cells · 2024Review
- Exploration of lncRNA/circRNA-miRNA-mRNA network in patients with chronic atrophic gastritis in Tibetan plateau areas based on DNBSEQ-G99 RNA sequencing.Scientific reports · 2024Article
- CD276-dependent efferocytosis by tumor-associated macrophages promotes immune evasion in bladder cancer.Nature communications · 2024Article
- Role and research progress of spasmolytic polypeptide‑expressing metaplasia in gastric cancer (Review).International journal of oncology · 2024Article
- Bridging Chronic Inflammation and Digestive Cancer: The Critical Role of Innate Lymphoid Cells in Tumor Microenvironments.International journal of biological sciences · 2024Review
- Apposition of Fibroblasts With Metaplastic Gastric Cells Promotes Dysplastic Transition.Gastroenterology · 2023Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
In the stomach, chronic inflammation causes metaplasia and creates a favorable environment for the evolution of gastric cancer. Glucocorticoids are steroid hormones that repress proinflammatory stimuli, but their role in the stomach is unknown. In this study, we show that endogenous glucocorticoids are required to maintain gastric homeostasis. Removal of circulating glucocorticoids in mice by adrenalectomy resulted in the rapid onset of spontaneous gastric inflammation, oxyntic atrophy, and spasmolytic polypeptide-expressing metaplasia (SPEM), a putative precursor of gastric cancer. SPEM and oxyntic atrophy occurred independently of lymphocytes. However, depletion of monocytes and macrophages by clodronate treatment or inhibition of gastric monocyte infiltration using the Cx3cr1 knockout mouse model prevented SPEM development. Our results highlight the requirement for endogenous glucocorticoid signaling within the stomach to prevent spontaneous gastric inflammation and metaplasia, and suggest that glucocorticoid deficiency may lead to gastric cancer development.
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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.