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Claudin Family Participates in the Pathogenesis of Inflammatory Bowel Diseases and Colitis-Associated Colorectal Cancer

期刊

FRONTIERS IN IMMUNOLOGY
卷 10, 期 -, 页码 -

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2019.01441

关键词

inflammatory bowel diseases; claudin; intestinal permeability; colitis-associated colorectal cancer; protein family

资金

  1. National Natural Science Foundation of China [81870374, 81670498]
  2. Pearl River S&T Nova Program of Guangzhou [201610010126]
  3. Guangdong Science and Technology [2017A030306021]
  4. Science and Technology Innovation Young Talents of Guangdong Special Support Plan [2016TQ03R296]

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Claudins are a multigene transmembrane protein family comprising at least 27 members. In gastrointestinal tract, claudins are mainly located in the intestinal epithelia; many types of claudins form a network of strands in tight junction plaques within the intercellular space of neighboring epithelial cells and build paracellular selective channels, while others act as signaling proteins and mediates cell behaviors. Claudin dysfunction may contribute to epithelial permeation disorder and multiple intestinal diseases. Over recent years, the importance of claudins in the pathogenesis of inflammatory bowel diseases (IBD) has gained focus and is being investigated. This review analyzes the expression pattern and regulatory mechanism of claudins based on existing evidence and elucidates the fact that claudin dysregulation correlates with increased intestinal permeability, sustained activation of inflammation, epithelial-to-mesenchymal transition (EMT), and tumor progression in IBD as well as consequent colitis-associated colorectal cancer (CAC), possibly shedding new light on further etiologic research and clinical treatments.

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