Spasmolytic polypeptide/TFF2-expressing metaplasia is a mucous-secreting reparative lineage that emerges at the ulcer margin after in response to gastric injury. Under conditions of chronic inflammation with parietal cell loss, SPEM has been found to emerge and evolve into neoplasia. Cluster-of-differentiation gene 44 (CD44) is known to coordinate normal and metaplastic epithelial cell proliferation. In particular, CD44 variant isoform 9 (CD44v9) associates with the cysteine-glutamate transporter xCT, stabilizes the protein and provides defense against reactive oxygen species (ROS). xCT stabilization by CD44v9 leads to defense against ROS by cysteine uptake, glutathione (GSH) synthesis, and maintenance of the redox balance within the intracellular environment. Furthermore, p38 signaling is a known downstream ROS target leading to diminished cell proliferation and migration - two vital processes of gastric epithelial repair. CD44v9 emerges during repair of the gastric epithelium after injury where it is co-expressed with other markers of SPEM. The regulatory mechanisms for the emergence of CD44v9 and the role of CD44v9 during the process of gastric epithelial regeneration are largely unknown. Inflammation and M2 macrophage infiltration have recently been demonstrated to play key role in the induction of SPEM after injury. The following review proposes new insights into the functional role of metaplasia in the process of gastric regeneration in response to ulceration. Our insights are extrapolated from documented studies reporting oxyntic atrophy and SPEM development, and our current unpublished findings using the acetic acid-induced gastric injury model.

中文翻译：

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化生在胃再生过程中的作用。

解痉多肽/TFF2 表达化生是一种分泌粘液的修复谱系，在胃损伤后出现在溃疡边缘。在伴有壁细胞丢失的慢性炎症条件下，已发现 SPEM 出现并演变为瘤形成。已知分化簇基因 44 (CD44) 可协调正常和化生上皮细胞增殖。特别是，CD44 变异亚型 9 (CD44v9) 与半胱氨酸-谷氨酸转运蛋白 xCT 结合，稳定蛋白质并提供对活性氧 (ROS) 的防御。CD44v9 对 xCT 的稳定导致通过半胱氨酸摄取、谷胱甘肽 (GSH) 合成和细胞内环境中氧化还原平衡的维持来防御 ROS。此外，p38 信号是已知的下游 ROS 目标，导致细胞增殖和迁移减少 - 胃上皮修复的两个重要过程。CD44v9 在损伤后胃上皮修复过程中出现，与其他 SPEM 标志物共表达。CD44v9 出现的调控机制和 CD44v9 在胃上皮再生过程中的作用在很大程度上是未知的。最近已证明炎症和 M2 巨噬细胞浸润在损伤后诱导 SPEM 中起关键作用。以下综述对化生在胃溃疡再生过程中的功能作用提出了新见解。我们的见解是从报告泌酸萎缩和 SPEM 发展的文献研究中推断出来的，