Maleki Navid, Mohammadzadeh Alireza, Mardaneh Jalal, Pazoki Hossein, Nattagh-Eshtivani Elyas
Student Research Committee, Infectious Diseases Research Center, Gonabad University of Medical Sciences, Gonabad, Iran.
Department of Microbiology, Faculty of Medicine, Infectious Diseases Research Center, Gonabad University of Medical Sciences, Gonabad, Iran.
Metabol Open. 2025 Aug 11;27:100385. doi: 10.1016/j.metop.2025.100385. eCollection 2025 Sep.
() infection is a globally prevalent gastrointestinal pathogen increasingly linked to various extra-gastric non-communicable diseases (NCDs). This review addresses the guiding question: What epidemiological and mechanistic links explain the association between H. pylori infection and chronic conditions such as cardiovascular disease (CVD), metabolic dysfunction-associated steatotic liver disease (MASLD), and type 2 diabetes mellitus (T2DM)? The manuscript synthesizes evidence from epidemiological studies and mechanistic research. In CVD, exacerbates chronic vascular inflammation, endothelial dysfunction, and autoimmune-like responses such as molecular mimicry. In MASLD, induces insulin resistance (IR), hepatic inflammation, and microbiota-mediated liver injury, although findings remain inconclusive across populations. For T2DM, multiple pathways including NLRP3 inflammasome activation, hormonal imbalances (e.g., ghrelin, leptin), and immune-genetic interactions involving TLR4 and SOCS3 suggest a role for in metabolic dysregulation and impaired glycemic control. While researchers have not yet fully elucidated causality, these findings indicate as a potential modifiable risk factor for NCDs. Future longitudinal and interventional studies are warranted to determine whether eradication of can mitigate chronic disease.
（幽门螺杆菌）感染是一种全球流行的胃肠道病原体，越来越多地与各种胃外非传染性疾病（NCDs）相关联。本综述探讨了以下指导性问题：哪些流行病学和机制联系解释了幽门螺杆菌感染与心血管疾病（CVD）、代谢功能障碍相关脂肪性肝病（MASLD）和2型糖尿病（T2DM）等慢性疾病之间的关联？本文综合了流行病学研究和机制研究的证据。在心血管疾病中，（幽门螺杆菌）会加剧慢性血管炎症、内皮功能障碍以及分子模拟等自身免疫样反应。在代谢功能障碍相关脂肪性肝病中，（幽门螺杆菌）会诱导胰岛素抵抗（IR）、肝脏炎症以及微生物群介导的肝损伤，尽管不同人群的研究结果尚无定论。对于2型糖尿病，包括NLRP3炎性小体激活、激素失衡（如胃饥饿素、瘦素）以及涉及Toll样受体4（TLR4）和细胞因子信号转导抑制因子3（SOCS3）的免疫遗传相互作用等多种途径表明（幽门螺杆菌）在代谢失调和血糖控制受损中发挥作用。虽然研究人员尚未完全阐明因果关系，但这些发现表明（幽门螺杆菌）是一种潜在的可改变的非传染性疾病风险因素。未来有必要进行纵向和干预性研究，以确定根除（幽门螺杆菌）是否可以减轻慢性疾病。
