| 黄威,潘晓娜,康玫,等.炎症性肠病与坏疽性脓皮病共病的研究演进与亚型特异性分子交叉机制剖析[J].安徽医药,待发表. |
| 炎症性肠病与坏疽性脓皮病共病的研究演进与亚型特异性分子交叉机制剖析 |
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| 投稿时间：2025-10-09 录用日期：2025-11-05 |
| DOI： |
| 中文关键词: 炎症性肠病 坏疽性脓皮病 文献计量学 生物信息学 精准医疗 |
| 英文关键词: |
| 基金项目:国家自然科学基金资助项目(No.82460108)；中国博士后科学基金(No.2025M772035) |
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| 中文摘要: |
| 目的 本研究旨在系统梳理炎症性肠病(Inflammatory Bowel Disease,IBD)与坏疽性脓皮病(Pyoderma Gangrenosum,PG)共病领域的研究演进趋势,并从亚型特异性角度深入揭示其分子交叉机制,以期为“肠-皮”轴互作机制提供新的理论依据,并为不同IBD亚型合并PG的精准防治提供分子分型基础。方法 整合文献计量学与生物信息学方法,检索2000–2025年8月31日间Web of Science核心合集相关文献,利用CiteSpace、VOSviewer等工具分析国家、机构、作者及关键词的合作网络与主题演进。进一步通过GeneCards与STRING数据库筛选IBD与PG的共享基因,构建蛋白质互作网络,并进行GO/KEGG通路富集分析,重点比较克罗恩病(Crohn"s Disease,CD)与溃疡性结肠炎(Ulcerative Colitis,UC)相关PG在分子机制上的异同。结果 文献计量分析显示该领域研究持续增长,欧美国家主导国际合作网络,中国虽发文量居前但国际合作与影响力较弱。生物信息学分析识别出236个IBD-PG共享基因,核心通路集中于“细胞因子-细胞因子受体相互作用”等炎症免疫相关过程。关键创新点在于发现CD背景下的PG显著富集于IL-17信号通路与志贺菌感染,而UC相关PG则突出富集于自然杀伤细胞介导的细胞毒性及耶尔森菌感染通路,揭示了两者在免疫启动机制上的亚型特异性差异。结论 本研究首次从多维度揭示IBD与PG共病具有“共性炎症基础、亚型特异通路”的双重特征。共病机制核心为“感染触发-固有免疫激活-细胞因子失衡-免疫细胞浸润”通路,而CD-PG与UC-PG在关键信号通路上存在明显差异。该发现不仅深化了对“肠-皮”轴互作机制的理解,也为基于IBD亚型的PG精准预防与靶向治疗提供了重要分子依据。 |
| 英文摘要: |
| Objective This study aims to systematically examine research trends in the comorbidity of Inflammatory Bowel Disease (IBD) and Pyoderma Gangrenosum (PG) and to elucidate their molecular cross-talk mechanisms from a subtype-specific perspective, thereby providing new theoretical insights into the "gut-skin axis" and a molecular basis for the precise management of PG in different IBD subtypes. Methods Integrating bibliometric and bioinformatic approaches, relevant publications from 2000 to 2025 (through August 31)were retrieved from the Web of Science Core Collection. Tools including CiteSpace and VOSviewer were employed to analyze collaborative networks and thematic evolution among countries, institutions, authors, and Keywords. Shared genes between IBD and PG were identified using GeneCards and STRING databases, followed by construction of protein-protein interaction networks and GO/KEGG enrichment analyses, with a focused comparison of molecular mechanisms between Crohn"s Disease (CD)-associated PG and Ulcerative Colitis (UC)-associated PG. Results Bibliometric analysis indicated sustained growth in this field, with European and American countries leading international collaborations. Although China ranked among the top publishing countries, its international collaboration and academic influence remained limited. Bioinformatic analysis identified 236 shared genes between IBD and PG, with core pathways significantly enriched in inflammation- and immune-related processes such as "cytokine-cytokine receptor interaction." Notably, the key finding revealed that PG in the context of CD was significantly associated with the IL-17 signaling pathway and Shigella infection, whereas UC-related PG was prominently enriched in natural killer cell-mediated cytotoxicity and Yersinia infection pathways, highlighting distinct immune activation mechanisms between the subtypes. Conclusion This study multi-dimensionally reveals the dual characteristics of IBD-PG comorbidity: common inflammatory foundations coupled with subtype-specific pathways. The core mechanism involves an "infection trigger–innate immune activation–cytokine dysregulation–immune cell infiltration" axis, while CD-PG and UC-PG exhibit significant differences in key signaling pathways. These findings not only deepen the understanding of the "gut-skin axis" interaction but also provide a crucial molecular basis for the precise prevention and targeted therapy of PG according to IBD subtypes. |
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