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肠道微生物群的变化与代谢功能障碍相关的脂肪肝炎和炎症性肠病:常见的致病特征
Giuseppe Guido Maria Scarlata1, Domenico Morano1, Abdulrahman Ismaiel2
1Department of Health Sciences, University of Catanzaro "Magna Graecia", 88100 Catanzaro, Italy.
Current issues in molecular biology
|October 28, 2025
概括
肠道微生物群失生症通过共享的炎症途径驱动代谢功能障碍相关的脂肪肝炎 (MASH) 和炎症性肠病 (IBD). 针对这些肠道微生物组的改变,可能为这两种疾病提供新的治疗策略.
科学领域:
- 微生物学 微生物学
- 胃肠病学 胃肠病学
- 免疫学 免疫学 免疫学
背景情况:
- 肠道微生物群失调与代谢功能障碍相关的脂肪肝炎 (MASH) 和炎症性肠病 (IBD) 有关.
- 共同的机制包括改变的短链脂肪酸生产,胆酸代谢和托代谢.
- 这些变化损害了肠道屏障的完整性,并激活了炎症通路.
研究的目的:
- 审查和综合当前关于肠道微生物群在MASH和IBD中的作用的证据.
- 突出MASH和IBD之间由肠道失调驱动的共享病原体机制.
- 为了强调微生物组向治疗的潜力.
主要方法:
- 现有文献的叙述性审查.
- 综合有关MASH和IBD肠道微生物群组成和功能的证据.
- 分析共享的分子和免疫路径.
主要成果:
- 在MASH和IBD中,失生症涉及有益细菌的丧失 (例如,Faecalibacterium prausnitzii) 和病原生物的丰富 (例如,Enterobacteriaceae).
- 共同的途径包括受损的丁酸盐可用性,改变的胆酸信号 (FXR,TGR5) 和缺陷的烯碳化合物受体激活.
- 微生物失调有助于表皮屏障功能障碍,全身炎症 (TNF-α,IL-6,TGF-β) 和器官特异性病理.
结论:
- 肠道微生物群通过共同的炎症轴在MASH和IBD的发病过程中发挥着中心作用.
- 肠肝和肠免疫轴代表了理解这些疾病的统一框架.
- 需要进一步的纵向,多主题研究来开发个性化,针对微生物组的治疗策略.
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