NAFLD and NASH: etiology, targets and emerging therapies.
Shulin Wei, Li Wang, Paul C Evans, Suowen Xu
Author Information
Shulin Wei: School of Life Sciences, Jilin University, Changchun, China; Department of Endocrinology, Institute of Endocrine and Metabolic Disease, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, Clinical Research Hospital of Chinese Academy of Sciences (Hefei), University of Science and Technology of China, Hefei, China.
Li Wang: Department of Biomedical Sciences, City University of Hong Kong, China.
Paul C Evans: Centre for Biochemical Pharmacology, William Harvey Research Institute, Barts and The London Faculty of Medicine and Dentistry, Queen Mary University of London, EC1M 6BQ, UK.
Suowen Xu: Department of Endocrinology, Institute of Endocrine and Metabolic Disease, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, Clinical Research Hospital of Chinese Academy of Sciences (Hefei), University of Science and Technology of China, Hefei, China. Electronic address: sxu1984@ustc.edu.cn.
Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) pose a significant threat to human health and cause a tremendous socioeconomic burden. Currently, the molecular mechanisms of NAFLD and NASH remain incompletely understood, and no effective pharmacotherapies have been approved. In the past five years, significant advances have been achieved in our understanding of the pathomechanisms and potential pharmacotherapies of NAFLD and NASH. Research advances include the investigation of the effects of the fibroblast growth factor 21 (FGF21) analog pegozafermin and the thyroid hormone receptor-β (THRβ) agonist resmetriom on hepatic fat content, NASH resolution and/or fibrosis regression. Future directions of NAFLD and NASH research (including combination therapy, organoids and humanized mouse models) are also discussed in this state-of-the-art review.
