title: Kupffer cells: increasingly significant role in nonalcoholic fatty liver disease.
abstract: Non-alcoholic fatty liver disease (NAFLD) is considered to be a manifestation of liver metabolic damage and is related to insulin resistance and genetic susceptibility. Inflammation mediated by Kupffer cells (KCs) is of critical importance to the development of NAFLD. The primary role of KCs in NAFLD is considered to be the perturbation of the C-Jun N-terminal kinase (JNK) and nuclear factor-kappa B (NF-κB) pathways as a result of lipopolysaccharide (LPS) recognition by Toll-like receptor 4 (TLR4). Simultaneously, the activation of NF-κB, as mediated by oxidative and endoplasmic reticulum (ER) stress and free fatty acid (FFA) or free cholesterol (FC) crystal formation, heavily relies on NF-κB regulatory factors and TLR4. Additionally, the imbalance of certain pro-inflammatory cytokines and chemokines released by innate immunity is deemed to promote the steatosis of hepatocytes. In conclusion, this review indicates that the inflammatory and oxidative stress of KCs play a significant role in the development of NAFLD.
authors.affiliation: Chongqing Key Laboratory of Hepatobiliary Surgery and Department of Hepatobiliary Surgery, Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
authors.forename: Zhang
authors.initials: Z
authors.lastname: Wenfeng
authors.affiliation: Chongqing Key Laboratory of Hepatobiliary Surgery and Department of Hepatobiliary Surgery, Second Affiliated Hospital, Chongqing Medical University, Chongqing, China; Department of Hepatobiliary Surgery, Suining Central Hospital, Suining, Sichuan, P. R. China.
authors.forename: Wu
authors.initials: W
authors.lastname: Yakun
authors.affiliation: Department of Infectious Diseases, Institute for Viral Hepatitis, Key Laboratory of Molecular Biology for Infectious Diseases, Ministry of Education, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, P. R. China.
authors.forename: Mu
authors.initials: M
authors.lastname: Di
authors.affiliation: Chongqing Key Laboratory of Hepatobiliary Surgery and Department of Hepatobiliary Surgery, Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
authors.forename: Gong
authors.initials: G
authors.lastname: Jianping
authors.affiliation: Chongqing Key Laboratory of Hepatobiliary Surgery and Department of Hepatobiliary Surgery, Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
authors.forename: Wu
authors.initials: W
authors.lastname: Chuanxin
authors.affiliation: Chongqing Key Laboratory of Hepatobiliary Surgery and Department of Hepatobiliary Surgery, Second Affiliated Hospital, Chongqing Medical University, Chongqing, China; Chongqing Three Gorges Medical College, Wanzhou, Chonqing, P.R. China.
authors.forename: Huang
authors.initials: H
authors.lastname: Chun
mesh_terms: D000818:Animals; D002784:Cholesterol / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D007728:Kupffer Cells / Q000378:metabolism* / Q000473:pathology; D008099:Liver / Q000378:metabolism* / Q000473:pathology; D065626:Non-alcoholic Fatty Liver Disease / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D018384:Oxidative Stress; D015398:Signal Transduction
chemical_list: D005230:Fatty Acids, Nonesterified; D018836:Inflammation Mediators; D002784:Cholesterol