Ask about this productRelated genes to: TFF2 protein
- Gene:
- TFF2 NIH gene
- Name:
- trefoil factor 2
- Previous symbol:
- SML1
- Synonyms:
- -
- Chromosome:
- 21q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1991-12-13
- Date modifiied:
- 2015-08-26
Related products to: TFF2 protein
Related articles to: TFF2 protein
- Spasmolytic polypeptide-expressing metaplasia (SPEM) arises in the gastric corpus in response to oxyntic atrophy, but its cellular origin and role in gastric cancer remain unclear. - Source: PubMed
Publication date: 2026/04/14
Tu RuhongZheng Hua-LongZheng BiyunZhong QingQian JinYu QianWu FeijingShiokawa ToshiroOchiai YosukeKobayashi HirokiWaterbury Quin TZamechek LeahGao YouxinTakahashi SatoruMizuno SeiyaHuang Chang MingLi PingHayakawa YokuWang Timothy C - Chronic atrophic gastritis (CAG) severity risk assessment remains challenging due to limitations of current static histologic/endoscopic tools. We evaluated the leucine-rich repeat-containing G-protein coupled receptor 5 (LGR5)/trefoil factor 2 (TFF2) ratio - quantifying gastric stem cell niche imbalance- as a dynamic biomarker for high-risk CAG (OLGA/OLGIM III-IV). - Source: PubMed
Publication date: 2026/04/09
Zhang QingqingWu DiGuo FengyunYang ShengnanBao LijingZhang RuiyingWang Ping - In clinical practice, Hezi Qingyou Formula (HZQYF) has been observed to effectively alleviate clinical symptoms associated with gastri ulcers, though its precise mechanism of action remains unclear. To investigate the effects of HZQYF on gastric ulcers, we established a rat model of gastric ulcer and examined its impact on ulcer area, pathological changes, inflammatory cytokines, gastric repair factors, levels of T-superoxide dismutase (SOD), and malondialdehyde (MDA), as well as metabolites in gastric tissue and feces. The results demonstrated that HZQYF significantly reduced the gastric ulcer area and promoted gastric tissue repair in rats. It downregulated the phosphorylation of P-P38, P-JNK1/2, and ERK1/2 proteins in the mitogen-activated protein kinases (MAPKs) pathway, inhibited pro-inflammatory cytokines such as interleukin (IL)-6, IL-1β, and tumor necrosis factor-α (TNF-α), enhanced the expression of gastric repair factors including vascular endothelial growth factor (VEGF), epidermal growth factor (EGF), trefoil factor family 2 (TFF2), and prostaglandin E2 (PGE2), reduced MDA content, and increased the activity of the antioxidant enzyme T-SOD, thereby suppressing inflammatory responses and ameliorating gastric mucosal damage. Metabolomic studies revealed that HZQYF effectively normalized 40 metabolites in gastric tissue through four key metabolic pathways and 39 metabolites in feces through five key metabolic pathways. Notably, it regulated taurine and hypotaurine metabolism, as well as phenylalanine metabolism, restoring metabolite levels to normal and ameliorating metabolic disorders in diseased rats. In conclusion, HZQYF promotes the healing of experimental gastric ulcers in rats through anti-inflammatory effects, activation of gastric repair factors, and normalization of gastric tissue metabolites, suggesting its potential therapeutic role in the treatment of gastric ulcers. - Source: PubMed
Feng ZhongWei RuixiaTian JunhaoLi HuiChen HaoboHao YajieChen MeiyunSu BingmeiLai YuqianXun MingjinZhang GuiminYao Meicun - Observational studies suggest that plasma proteins play a crucial role in the development and progression of obstructive sleep apnea (OSA); however, the causal relationship between plasma proteins and OSA remains controversial. This study conducted a comprehensive evaluation of the causal relationships between 4,907 plasma proteins and OSA by employing bidirectional Mendelian randomization (MR) analysis, network pharmacology strategies, and single-cell sequencing techniques. The plasma protein data used in this study were derived from Ferkingstad et al.'s research (n = 35,559), and OSA-related data were obtained from genome-wide association studies (GWAS) conducted on European populations through Finland's biobank (FinnGen). This study utilized multi-omics integration strategies, including enrichment analysis, protein-protein interaction (PPI) network construction, drug target prediction, molecular docking simulation, and single-cell transcriptome sequencing, to investigate the biological mechanisms of identified targets and evaluate their potential applications in drug development. MR analysis identified 62 plasma proteins significantly associated with OSA risk, including NTN4 (p = 0.003, OR = 1.076, CI [1.024, 1.129]) and TFF2 (p = 0.004, OR = 1.098, CI [1.029, 1.174]). Further reverse Mendelian analysis revealed causal relationships between OSA and the CELF2, NTRK3, ANTXR2, and MYOM2 genes. PPI network analysis identified 10 core genes, including IL1β, TGFβ1, EGF, SHH, and SMAD2, which participate in critical pathological processes in OSA, such as oxidative stress, inflammatory responses, and immune regulation. Through drug prediction analysis, this study identified compounds with potential therapeutic effectiveness, including 3,4-DHB, BIM IX, and 1,9-Pyrazoloanthrone, and molecular docking studies further confirmed their high binding affinity to target proteins. Single-cell sequencing revealed high expression levels of key genes in T cells and dendritic cells, thereby confirming the critical role of these cells in the pathological progression of OSA. A total of 62 candidate therapeutic targets for OSA were identified in this study, with 10 of these targets deemed important candidates for clinical trials. These findings not only enrich the understanding of the molecular pathological mechanisms underlying OSA but also offer new perspectives for developing targeted therapeutic strategies to treat the condition. By facilitating the establishment of more precise and personalized disease management approaches, these results are expected to advance the development of therapeutic drugs for OSA and substantially reduce the economic costs associated with new drug development. - Source: PubMed
Publication date: 2026/02/19
Duan LingzhiWang YanJing HaiqingWang YanqiongNing ShuyeYang ZhengfuZhang Aihua - Gastric mucosal integrity is essential for maintaining systemic homeostasis, serving as the primary defense against external insults. Ethanol ingestion is a major clinical cause of gastric mucosal injury, yet effective prevention or treatment remains limited. This study investigates the protective role of nitrate against ethanol-induced gastric ulcers and its underlying mechanisms. In vivo, nitrate significantly ameliorated ethanol-induced gastric bleeding, edema, inflammation, and mucus layer thinning in rats, while strengthening the vascular endothelial barrier. Transcriptomic analyses and trefoil factor 2 (Tff2)-knockdown rats experiment identified as the key gene responsible for mediating nitrate's protective effects against ethanol. In vitro, TFF2 was found to be a crucial target for nitrates, which enhance the migratory reparative capacities of human gastric epithelial cells. Further assays revealed that RBPJ regulates the TFF2 promoter, and NICD-RBPJ complex formation is critical for TFF2 transcriptional repression. We demonstrate for the first time that TFF2 is a central effector in nitrate-mediated gastric mucosal defense and repair and implicate the Notch signaling pathway in TFF2 regulation. These findings suggest nitrate exerts a protective effect on the gastric mucosa through multiple ways. TFF2 modulation as a potential preventive strategy for ethanol-induced gastric ulcers. - Source: PubMed
Publication date: 2026/02/05
Liu YingWen XinLin YuxuanZhang ChunmeiWang JinsongSun GuangyongZhang DongYan RenhongChen MoWang SonglinLi Shaorong