Breaking Barriers in Functional Dyspepsia: A Systematic Review and Meta-analysis on Duodenal Tight Junction Protein Expression.

IF 3.3 3区 医学 Q2 CLINICAL NEUROLOGY Journal of Neurogastroenterology and Motility Pub Date : 2024-07-30 DOI:10.5056/jnm24013
Radu A Farcas, Malaz Almasri, Simona Grad, Stefan-Lucian Popa, Daniel C Leucuta, Abdulrahman Ismaiel, Dan L Dumitrascu
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Abstract

Background/aims: Disruptions in tight junction (TJ) protein expression leading to duodenal epithelial barrier impairment may contribute to increased intestinal permeability, potentially playing a role in functional dyspepsia (FD) pathophysiology. Currently published studies evaluated the role of several TJ proteins in FD patients with inconsistent results. Therefore, we conducted this systematic review and metaanalysis to evaluate the duodenal mucosal expression of several TJ proteins in FD.

Methods: We performed a systematic electronic search on PubMed, EMBASE, and Scopus using predefined keywords. Diagnosis of FD by Rome III or Rome IV criteria was considered acceptable. Full articles satisfying our inclusion and exclusion criteria were included. The principal summary outcome was the mean difference of several TJ proteins in FD patients and control subjects.

Results: A total of 8 and 5 studies were included in our qualitative and quantitative synthesis, respectively, with a total population of 666 participants, out of which 420 were FD patients. No significant differences were observed between FD patients and controls in the expression of claudin-1 (-0.102 [95% CI, -0.303, 0.099]), claudin-2 (0.161 [95% CI, -0.134, 0.456)], claudin-3 (0.278 [95% CI, -0.280, 0.837]), claudin-4 (0.045 [95% CI, -0.264, 0.354]), ZO-1 (-0.221 [95% CI, -0.683, 0.241]), ZO-2 (-0.070 [95% CI, -0.147, 0.007]), ZO-3 (-0.129 [95% CI, -0.376, 0.118]), β-catenin (-0.135 [95% CI, -0.484, 0.214]), E-cadherin (-0.083 [95% CI, -0.229, 0.063]), and occludin (-0.158 [95% CI, -0.409, 0.093]).

Conclusions: The expressions of all evaluated proteins including claudin-1, claudin-2, claudin-3, claudin-4, ZO-1, ZO-2, ZO-3, β-catenin, E-cadherin, and occludin did not significantly differ between FD patients and controls. However, due to the limited number of included studies, results should be interpreted with caution.

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打破功能性消化不良的障碍:关于十二指肠紧密连接蛋白表达的系统回顾和元分析。
背景/目的:致十二指肠上皮屏障受损的紧密连接(TJ)蛋白表达紊乱可能会导致肠道通透性增加,并可能在功能性消化不良(FD)病理生理学中发挥作用。目前已发表的研究评估了几种 TJ 蛋白在 FD 患者中的作用,但结果并不一致。因此,我们进行了这一系统综述和荟萃分析,以评估 FD 中几种 TJ 蛋白的十二指肠粘膜表达:我们使用预定义的关键词在 PubMed、EMBASE 和 Scopus 上进行了系统的电子检索。根据罗马III或罗马IV标准诊断为FD者均可接受。符合纳入和排除标准的文章均被纳入。主要的总结性结果是 FD 患者和对照组中几种 TJ 蛋白的平均差异:我们的定性和定量综述分别共纳入了 8 项和 5 项研究,参与研究的总人数为 666 人,其中 420 人为 FD 患者。FD患者和对照组在claudin-1(-0.102 [95% CI, -0.303, 0.099])、claudin-2(0.161 [95% CI, -0.134, 0.456)]、claudin-3(0.278 [95% CI, -0.280, 0.837])、claudin-4(0.045 [95% CI, -0.264, 0.354])、ZO-1(-0.221 [95% CI, -0.683, 0.241])、ZO-2(-0.070 [95% CI, -0.147, 0.007])、ZO-3(-0.129 [95% CI, -0.376, 0.118])、β-catenin(-0.135 [95% CI, -0.484, 0.214])、E-cadherin (-0.083 [95% CI, -0.229, 0.063])和 occludin (-0.158 [95% CI, -0.409, 0.093]).结论:结论:FD患者和对照组的所有评估蛋白(包括claudin-1、claudin-2、claudin-3、claudin-4、ZO-1、ZO-2、ZO-3、β-catenin、E-cadherin和occludin)的表达均无显著差异。然而,由于纳入的研究数量有限,在解释结果时应谨慎。
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来源期刊
Journal of Neurogastroenterology and Motility
Journal of Neurogastroenterology and Motility GASTROENTEROLOGY & HEPATOLOGY-CLINICAL NEUROLOGY
CiteScore
6.30
自引率
8.80%
发文量
96
期刊介绍: Journal of Neurogastroenterology and Motility (J Neurogastroenterol Motil) is a joint official journal of the Korean Society of Neurogastroenterology and Motility, the Thai Neurogastroenterology and Motility Society, the Japanese Society of Neurogastroenterology and Motility, the Indian Motility and Functional Disease Association, the Chinese Society of Gastrointestinal Motility, the South East Asia Gastro-Neuro Motility Association, the Taiwan Neurogastroenterology and Motility Society and the Asian Neurogastroenterology and Motility Association, launched in January 2010 after the title change from the Korean Journal of Neurogastroenterology and Motility, published from 1994 to 2009.
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