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Ulcerative colitis:signaling pathways,therapeutic targets and interventional strategies
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作者 Jinhao Jia Ying Liu +5 位作者 Dan Wang Zhaohai Pan Qiusheng Zheng Jun Lu Chao Liang Defang Li 《Signal Transduction and Targeted Therapy》 2026年第3期1319-1354,共36页
Ulcerative colitis(UC)is the most common chronic inflammatory disease of the intestinal tract in clinical practice,and long-term chronic inflammation leads to repeated damage to and repair of the colonic mucosa,which ... Ulcerative colitis(UC)is the most common chronic inflammatory disease of the intestinal tract in clinical practice,and long-term chronic inflammation leads to repeated damage to and repair of the colonic mucosa,which may progress to malignancy through atypical hyperplasia.However,there are currently no fully targeted drugs for the treatment of UC.In this review,we discuss several cellular processes,such as autophagy,endoplasmic reticulum stress,mitochondrial dysfunction,macrophage polarization,ferroptosis and the Th/Treg cell balance,which are associated with the occurrence and development of UC.Many molecular targets and signaling pathways,such as nuclear factor kappa-B(NF-κB),phosphatidylinositol 3 kinase/protein kinase B(PI3K/AKT),Wnt/β-catenin,adenosine 5’-monophosphate-activated protein kinase(AMPK),toll-like receptor(TLR),Janus kinase/signal transducer and activator of transcription(JAK/STAT),long noncoding RNAs(lncRNAs),and microRNAs(miRNAs),play crucial roles in the progression of UC.We also summarize the common treatment strategies for UC,including lifestyle interventions,aminosalicylic acid preparations,corticosteroid drugs,biologics,fecal microbiota transplantation,and other drugs for symptomatic treatment.This review provides a detailed theoretical basis for the pathology and treatment of UC.Future research could focus on optimizing the treatment plan and achieving more precise and personalized treatment with multiple targets in multiple aspects. 展开更多
关键词 atypical hyperplasiahoweverthere colonic mucosawhich chronic inflammatory disease signaling pathways autophagyendoplasmic reticulum stressmitochondrial dysfunctionmacrophage polarizationferroptosis ulcerative colitis uc cellular processessuch ulcerative colitis
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