Related Experiment Video
Updated: Jan 12, 2026
Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
Published on: February 20, 2019
Cellular lineage origins of spasmolytic polypeptide-expressing metaplasia (SPEM): persistent and intensifying debates
Xiaofeng Li1, Yu Li2, Lili Wu3
1First Clinical Medical College, Heilongjiang University of Chinese Medicine, Harbin, China.
Abstract:
Spasmolytic Polypeptide-Expressing Metaplasia (SPEM) is a gastric fundic gland metaplasia resembling deep antral glands, associated with drug injury, Helicobacter pylori (H. pylori), or bile reflux. Early-stage SPEM acts as a reparative response, but if the damaging stimuli persist, the metaplastic changes may become irreversible, raising the risk of gastric cancer development. Traditionally, SPEM arises via passive transdifferentiation of chief cells following parietal cell loss. However, recent lineage tracing and genetic models challenge this, suggesting active depletion of chief cells and involvement of isthmus stem cells also contribute to SPEM development, intensifying debate over its cellular origins. This review synthesizes SPEM's physicochemical drivers and critically evaluates evidence for the three proposed sources: (1) passive chief cell transdifferentiation (2), active chief cell loss, and (3) isthmus stem cells. Clarifying the heterogeneity in the origin of SPEM is challenging until more specific cell ablation techniques are developed, but timely classification of existing research may be instructive.
Insights
Spasmolytic Polypeptide-Expressing Metaplasia (SPEM) arises from gastric injury. Current research debates whether SPEM originates from passive chief cell changes or active chief cell loss and stem cell involvement.
Area of Science:
- Gastroenterology
- Cell Biology
- Oncology
Background:
- Spasmolytic Polypeptide-Expressing Metaplasia (SPEM) is a gastric metaplasia linked to injury, Helicobacter pylori, and bile reflux.
- SPEM is a risk factor for gastric cancer development if damaging stimuli persist.
- The cellular origins of SPEM are debated, with traditional views challenged by recent findings.
Purpose of the Study:
- To review the physicochemical drivers of SPEM.
- To critically evaluate the proposed cellular origins of SPEM.
- To synthesize current research on SPEM development.
Main Methods:
- Literature review and synthesis of existing research.
- Critical evaluation of evidence for different cellular origins.
- Analysis of physicochemical factors contributing to SPEM.
Main Results:
- SPEM can arise from passive chief cell transdifferentiation, active chief cell depletion, or isthmus stem cell involvement.
- Evidence suggests multiple pathways contribute to SPEM development, indicating heterogeneity.
- Further research with specific cell ablation techniques is needed to clarify SPEM origins.
Conclusions:
- The cellular origin of SPEM is complex and likely involves multiple mechanisms.
- Understanding SPEM's heterogeneous origins is crucial for assessing gastric cancer risk.
- Classifying current research is essential for guiding future investigations into SPEM.
