Role of Neurite Outgrowth Inhibitor B Receptor in hepatic steatosis.

Fangzhi Chen, Zhongcheng Mo, Qiaoqing Zhong, Ming Li

Journal: Acta histochemica 2022;124(8):151977

PMID: 36423390

Full Text on Elsevier Science View on PubMed

Abstract

Hepatic steatosis, characterized by excessive lipid accumulation, is one of the common liver diseases. Neurite Outgrowth Inhibitor B Receptor (NgBR) regulates the lipid metabolism, cholesterol efflux, and protein glycosylation. Recently, it has been demonstrated that NgBR deficiency leads to hepatic steatosis. In this review we summarize the current knowledge about the structure of NgBR, the role and molecular mechanism of NgBR in the occurrence and development of hepatic steatosis.

Address: The Second Affiliated Hospital, Department of Gastroenterology, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.; Guangxi Key Laboratory of Molecular Medicine in Liver Injury and Repair, Guilin Medical University, Guilin 541001, Guangxi, China.; Department of Anesthesia, Critical Care & Pain Med, Beth Israel Deaconess Medical Center, Harvard University, Boston, MA 02115, USA; Department of Cardiovascular Medicine, Xiangya Hospital, Central South University, Changsha 410008, China. Electronic address: [email protected].; Hunan Province Key Laboratory for Antibody-based Drug and Intelligent Delivery System, Hunan University of Medicine, Huaihua 418000, Hunan, China. Electronic address: [email protected].

DOI: 10.1016/j.acthis.2022.151977

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MeSH Terms: Humans, Fatty Liver, Lipid Metabolism, Neuronal Outgrowth