Corrigendum to "ATF4- and CHOP-Dependent Induction of FGF21 through Endoplasmic Reticulum Stress".

Xiao-Shan Wan,Xiao-Kun Li,Huiping Zhou,Xuan Wang,Jian Xiao

doi:10.1155/2018/3218606

Abstract

[This corrects the article DOI: 10.1155/2014/807874.].

Highlights

The fibroblast growth factor family contains 22 members with a wide range of biological functions relevant to regulating cell growth, differentiation, wound healing, development, BioMed Research International and angiogenesis [1–3]
It has been reported that serum Fibroblast growth factor 21 (FGF21) and hepatic mRNA expression levels in patients with nonalcoholic fatty liver disease (NAFLD) are significantly higher than those in control subjects, which correlates with a substantial increase in hepatic triglyceride levels [14–16]
Similar to activating transcription factor 4 (ATF4), CCAAT enhancer binding protein homologous protein (CHOP) overexpression significantly increased the FGF21 promoter activity. These findings indicate that both ATF4 and CHOP are involved in Endoplasmic reticulum (ER) stress-induced activation of FGF21 transcription

Summary

Introduction

The fibroblast growth factor family contains 22 members with a wide range of biological functions relevant to regulating cell growth, differentiation, wound healing, development, BioMed Research International and angiogenesis [1–3]. It has been reported that serum FGF21 and hepatic mRNA expression levels in patients with NAFLD are significantly higher than those in control subjects, which correlates with a substantial increase in hepatic triglyceride levels [14–16]. Animal studies showed that serum FGF21 concentrations and FGF21 mRNA levels in the liver and adipose tissue of high fat diet-induced and genetically modified obese mice are higher compared with those in wild-type mice [6, 8, 22]. Under various stress conditions, FGF21 is increased, for example, in individuals who either are overweight or have type 2 diabetes, or NAFLD. These observations suggest that the increased FGF21 levels in metabolic diseases may be due to feedback regulation.

Methods

Results

Conclusion