Frontiers in cell and developmental biology · 2026
The mechanical niche in gastric precancer: extracellular matrix remodeling, mechanotransduction, and stem-cell fate.
СтатьяОбзорНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Hu Lanshuo, Huang Xuanchun, Zhang Tai, Wu Yeqian, Yang Liangjun, Zhu Jiajie, Tang Xudong, Fei Baoying
Аннотация
BACKGROUND: The Correa cascade foregrounds infection, inflammation, and epithelial change but does not fully explain how the physical tissue environment influences progression from atrophy to metaplasia and dysplasia.
METHODS: We integrated human observations, gastric organoid and animal perturbation studies, advanced gastric-cancer experiments, and cross-tissue evidence using the Gastric Precancer Mechanobiology Evidence Stratification framework, which ranks evidence by proximity to causal human precancerous mechanics.
RESULTS: Direct human mechanical measurements remain sparse and methodologically heterogeneous, precluding a universal stiffening trajectory. YAP has the strongest functional support across gastric regeneration and metaplastic remodeling, integrin-adhesion signaling is convergent but mechanically under-specified, and Piezo1 evidence derives mainly from advanced cancer. Three non-exclusive models-mechanical driver, epithelial-first remodeling, and inflammation-mediated feedback-produce distinct temporal predictions.
CONCLUSION: Gastric precancer is best understood through a mechanically extended Correa framework in which static matrix properties, dynamic loading, regional anatomy, inflammatory context, and lineage state jointly determine whether injury resolves or stabilizes abnormal epithelial states. Spatial human mechanics linked to dynamic patient-derived perturbation models are required before mechanical biomarkers or pathway-directed interventions can guide clinical care.
METHODS: We integrated human observations, gastric organoid and animal perturbation studies, advanced gastric-cancer experiments, and cross-tissue evidence using the Gastric Precancer Mechanobiology Evidence Stratification framework, which ranks evidence by proximity to causal human precancerous mechanics.
RESULTS: Direct human mechanical measurements remain sparse and methodologically heterogeneous, precluding a universal stiffening trajectory. YAP has the strongest functional support across gastric regeneration and metaplastic remodeling, integrin-adhesion signaling is convergent but mechanically under-specified, and Piezo1 evidence derives mainly from advanced cancer. Three non-exclusive models-mechanical driver, epithelial-first remodeling, and inflammation-mediated feedback-produce distinct temporal predictions.
CONCLUSION: Gastric precancer is best understood through a mechanically extended Correa framework in which static matrix properties, dynamic loading, regional anatomy, inflammatory context, and lineage state jointly determine whether injury resolves or stabilizes abnormal epithelial states. Spatial human mechanics linked to dynamic patient-derived perturbation models are required before mechanical biomarkers or pathway-directed interventions can guide clinical care.