| Literature DB >> 35114889 |
Ricardo Diaz-Aragon1, Michael C Coard1, Sriram Amirneni1, Lanuza Faccioli1, Nils Haep1, Michelle R Malizio1, Takashi Motomura1, Zehra N Kocas-Kilicarslan1, Alina Ostrowska1,2, Rodrigo M Florentino1, Carla Frau1.
Abstract
The prevalence of end-stage liver disease (ESLD) in the US is increasing at an alarming rate. It can be caused by several factors; however, one of the most common routes begins with nonalcoholic fatty liver disease (NAFLD). ESLD is diagnosed by the presence of irreversible damage to the liver. Currently, the only definitive treatment for ESLD is orthotopic liver transplantation (OLT). Nevertheless, OLT is limited due to a shortage of donor livers. Several promising alternative treatment options are under investigation. Researchers have focused on the effect of liver-enriched transcription factors (LETFs) on disease progression. Specifically, hepatocyte nuclear factor 4-alpha (HNF4α) has been reported to reset the liver transcription network and possibly play a role in the regression of fibrosis and cirrhosis. In this review, we describe the function of HNF4α, along with its regulation at various levels. In addition, we summarize the role of HNF4α in ESLD and its potential as a therapeutic target in the treatment of ESLD.Entities:
Keywords: ESLD; HNF4α; LETFs; hepatocytes; molecular therapy
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Year: 2021 PMID: 35114889 PMCID: PMC9208774 DOI: 10.1080/15476278.2021.1994273
Source DB: PubMed Journal: Organogenesis ISSN: 1547-6278 Impact factor: 2.316