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慢性胃炎患者中[具体内容缺失]与血清缺氧诱导因子-1α、缺氧诱导因子-2α及人跨膜脯氨酰4-羟化酶活性的关联

Association of with Serum HIF-1α, HIF-2α, and Human Transmembrane Prolyl 4-Hydroxylase Activity in Patients with Chronic Gastritis.

作者信息

Ergün Sefa, Kutluk Fadime, Turgut Basar Can, Dumur Seyma, Sayılı Uğurcan, Ergun Dilek Duzgun, Uzun Hafize

机构信息

Department of General Surgery, Cerrahpaşa Faculty of Medicine, Istanbul University-Cerrahpasa, Istanbul 34320, Turkey.

Department of General Surgery, Istanbul Avcılar Murat Kölük State Hospital, Istanbul 34320, Turkey.

出版信息

Medicina (Kaunas). 2025 Jun 28;61(7):1174. doi: 10.3390/medicina61071174.

DOI:10.3390/medicina61071174
PMID:40731804
Abstract

: Chronic mucosal infection with () plays a key role in the development of gastroduodenal disorders such as chronic gastritis, peptic ulcers, gastric lymphoma, and gastric cancer by triggering local immune responses and inducing hypoxic and inflammatory conditions in the gastric mucosa. This study aims to evaluate the potential diagnostic value of hypoxia-inducible factors HIF-1α and HIF-2α, along with transmembrane prolyl 4-hydroxylase (P4H-TM), as biomarkers in -positive patients. Additionally, the study investigates the association between these markers and alterations in lipid profiles, as well as their involvement in the molecular mechanisms underlying gastric conditions like gastritis, particularly in the context of H. pylori infection. : This study was conducted at Istanbul Avcılar Murat Kölük State Hospital's General Surgery Outpatient Clinic. A total of 60 participants were included: 40 patients diagnosed with chronic gastritis (20 -positive and 20 -negative) and 20 healthy controls confirmed negative by 13C-urea breath test. Blood samples were collected for ELISA analysis of HIF-1α, HIF-2α, and P4H-TM levels. Additionally, lipid profiles were measured and compared among the groups. No significant differences were found among the groups in terms of demographic factors such as age, sex, or body mass index (BMI). However, significant variations were observed in the levels of HIF-1α, HIF-2α, and P4H-TM across all groups ( < 0.001 for each marker). These markers were substantially elevated in the -positive gastritis group compared to both the H. pylori-negative and healthy control groups. Receiver Operating Characteristic (ROC) curve analysis revealed that all evaluated markers exhibited strong diagnostic accuracy in differentiating H. pylori-positive individuals from other groups. HIF-1α (AUC: 0.983) and HIF-2α (AUC: 0.981) both achieved 100% sensitivity with specificities of 93.3% and 91.1%, respectively. P4H-TM showed an AUC of 0.927, with 85% sensitivity and 95.6% specificity. These findings indicate that HIF-1α, HIF-2α, and P4H-TM may serve as effective biomarkers for diagnosing -positive patients and may be linked to changes in lipid metabolism. The elevated expression of these markers in response to infection highlights their potential roles in the inflammatory and hypoxic pathways that contribute to the pathogenesis of gastric diseases such as gastritis.

摘要

幽门螺杆菌()慢性黏膜感染通过触发局部免疫反应并在胃黏膜中诱导缺氧和炎症状态,在慢性胃炎、消化性溃疡、胃淋巴瘤和胃癌等胃十二指肠疾病的发生发展中起关键作用。本研究旨在评估缺氧诱导因子HIF-1α和HIF-2α以及跨膜脯氨酰4-羟化酶(P4H-TM)作为幽门螺杆菌阳性患者生物标志物的潜在诊断价值。此外,该研究还调查了这些标志物与血脂谱变化之间的关联,以及它们在胃炎等胃部疾病潜在分子机制中的作用,特别是在幽门螺杆菌感染的背景下。:本研究在伊斯坦布尔阿夫西拉尔穆拉特·科吕克州立医院普通外科门诊进行。共纳入60名参与者:40名被诊断为慢性胃炎的患者(20名幽门螺杆菌阳性和20名幽门螺杆菌阴性)以及20名经13C-尿素呼气试验确认阴性的健康对照者。采集血样用于ELISA分析HIF-1α、HIF-2α和P4H-TM水平。此外,测量并比较了各组的血脂谱。在年龄、性别或体重指数(BMI)等人口统计学因素方面,各组之间未发现显著差异。然而,所有组中HIF-1α、HIF-2α和P4H-TM水平均观察到显著差异(每个标志物P<0.001)。与幽门螺杆菌阴性组和健康对照组相比,幽门螺杆菌阳性胃炎组中这些标志物显著升高。受试者操作特征(ROC)曲线分析显示,所有评估的标志物在区分幽门螺杆菌阳性个体与其他组方面均表现出较强的诊断准确性。HIF-1α(AUC:0.983)和HIF-2α(AUC:0.981)的敏感性均达到100%,特异性分别为93.3%和91.1%。P4H-TM的AUC为0.927,敏感性为85%,特异性为95.6%。这些发现表明,HIF-1α、HIF-

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本文引用的文献

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The Distinct Role of HIF-1α and HIF-2α in Hypoxia and Angiogenesis.缺氧诱导因子-1α(HIF-1α)和缺氧诱导因子-2α(HIF-2α)在缺氧和血管生成中的不同作用
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Molecular Mechanisms and Treatment Strategies for Helicobacter pylori-Induced Gastric Carcinogenesis and Mucosa-Associated Lymphoid Tissue (MALT) Lymphoma.幽门螺杆菌诱导胃癌发生及黏膜相关淋巴组织(MALT)淋巴瘤的分子机制与治疗策略
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Endothelial HIF-2α regulates murine pathological angiogenesis and revascularization processes.
内皮细胞缺氧诱导因子-2α调节小鼠病理性血管生成和血管再形成过程。
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