Regulation of Lipid Metabolism by Lamin in Mutation-Related Diseases

Yue Peng; Qianyu Tang; Fan Xiao; Nian Fu

doi:10.3389/fphar.2022.820857

Regulation of Lipid Metabolism by Lamin in Mutation-Related Diseases

Front Pharmacol. 2022 Feb 25:13:820857. doi: 10.3389/fphar.2022.820857. eCollection 2022.

Authors

Yue Peng¹, Qianyu Tang¹, Fan Xiao², Nian Fu^{1

2}

Affiliations

¹ The Affiliated Nanhua Hospital, Department of Gastroenterology, Hunan Provincial Clinical Research Center of Metabolic Associated Fatty Liver Disease, Hengyang, China.
² The Affiliated Nanhua Hospital, Clinical Research Institute, Hengyang Medical School, University of South China, Hengyang, China.

Abstract

Nuclear lamins, known as type 5 intermediate fibers, are composed of lamin A, lamin C, lamin B1, and lamin B2, which are encoded by LMNA and LMNB genes, respectively. Importantly, mutations in nuclear lamins not only participate in lipid disorders but also in the human diseases, such as lipodystrophy, metabolic-associated fatty liver disease, and dilated cardiomyopathy. Among those diseases, the mechanism of lamin has been widely discussed. Thereby, this review mainly focuses on the regulatory mechanism of the mutations in the lamin gene in lipid alterations and the human diseases. Considering the protean actions, targeting nuclear lamins may be a potent therapeutic avenue for lipid metabolic disorders and human diseases in the future.

Keywords: human diseases; lipid metabolism; lipodystrophy; mutation of lamin; nuclear lamins.

Publication types

Review