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Updated: Jun 20, 2026
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Mouse- and Human-derived Primary Gastric Epithelial Monolayer Culture for the Study of Regeneration
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THE ORIGINS AND PROGRESSION OF PYLORIC METAPLASIA FOLLOWING GASTRIC MUCOSAL INJURY.
Sophia K Cornish1,2, Eunyoung Choi3,1,4, Jason C Mills5
1Epithelial Biology Center, Vanderbilt University Medical Center, Nashville, TN, United States.
Physiological Reviews
|June 19, 2026
Summary
Deep gastric injury triggers metaplasia, a repair process where chief cells transform into spasmolytic polypeptide-expressing metaplasia (SPEM) cells. Persistent metaplasia, especially SPEM cells, increases gastric cancer risk.
Area of Science:
- Gastroenterology
- Cell Biology
- Oncology
Background:
- The gastric mucosa undergoes constant repair after injury.
- Deeper injuries can lead to persistent metaplasia, altering gland composition.
- Pyloric metaplasia involves expansion of foveolar, mucous neck, and SPEM cells.
Purpose of the Study:
- To review current knowledge on gastric metaplasia following deep mucosal injury.
- To discuss controversies and unanswered questions regarding metaplasia establishment and progression.
- To highlight the link between metaplasia and gastric cancer risk.
Main Methods:
- Review of existing literature on gastric mucosal injury and repair.
- Analysis of cellular dynamics and lineage transitions in metaplasia.
- Discussion of molecular mechanisms regulating chief cell transdifferentiation.
Main Results:
- Deep injury induces chief cell transdifferentiation into SPEM cells, aiding wound healing.
- Persistent metaplasia, driven by chronic inflammation or severe injury, can lead to intestinal metaplasia.
- Aberrant SPEM cell persistence promotes intestinal metaplasia, increasing gastric cancer risk.
Conclusions:
- Understanding metaplasia dynamics is crucial for identifying therapeutic targets.
- Further research is needed to uncover lineage transition markers.
- Targeting metaplasia progression may reduce gastric cancer incidence.
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