Therapeutic targeting of myeloid cells in liver fibrosis:Mechanisms and clinical prospects
Yue Wang1
Yiming Liu1
Dan Chen2
Leiming Liu3
Leimin Sun4
Lingling Zhang1
1.Department of Gastroenterology,Center for Metabolic Medicine,The Fourth Affiliated Hospital of School of Medicine,and International School of Medicine,International Institutes of Medicine,Zhejiang University,Yiwu,China;Department of Hematology,Center for Metabolic Medicine,The Fourth Affiliated Hospital of School of Medicine,and International School of Medicine,International Institutes of Medicine,Zhejiang University,Yiwu,China2.Department of Hematology,Center for Metabolic Medicine,The Fourth Affiliated Hospital of School of Medicine,and International School of Medicine,International Institutes of Medicine,Zhejiang University,Yiwu,China3.Key Laboratory of Artificial Organs and Computational Medicine in Zhejiang Province,Institute of Translational Medicine,Shulan International Medical College,Zhejiang Shuren University,Hangzhou,China4.Department of Gastroenterology,Sir Run Run Shaw Hospital,Zhejiang University School of Medicine,Hangzhou,China
摘要:Liver fibrosis,a hallmark pathological endpoint of chronic aging-related liver diseases,remains a clinical challenge with limited therapeutic options.In healthy liver,myeloid cells constitute<5%of total hepatic immune cells,primarily comprising tissue-resident Kupffer cells.However,during aging or chronic injury,bone marrow-derived myeloid cell recruitment increases by two-to threefold in murine fibrotic models,reaching 15%-20%of intrahepatic immune populations.These infiltrating myeloid subsets exhibit functional plasticity,dynamically differentiating into pro-inflammatory mac-rophages or fibrosis-promoting Kupffer-like cells,contingent upon chemokine gradi-ents(e.g.,CCL2/CCR2 axis)and damage-associated molecular patterns(DAMPs).This review systematically examines the regulatory mechanisms of myeloid cells in liver fibrogenesis,with particular emphasis on their developmental origins,hepatic recruit-ment dynamics,functional heterogeneity,and pathogenic contributions to fibrosis.Furthermore,signaling pathways involving myeloid cells in liver fibrosis and therapeu-tic approaches modulating their differentiation and recruitment are discussed in this review.
机标关键词:fibrosisclinicalcellslivermechanismsmyeloidprospectstargeting
论文发表日期:2025-07-30
在线出版日期:2025-09-28(本平台首次上网日期,不代表文献的发表时间)
页数:14( 1215-1228 )
英文信息展开
动物模型与实验医学(英文)

动物模型与实验医学(英文)

CSCD
ISSN:2096-5451
年,卷(期):2025,8(7)
所属栏目:Regular Article