Role of Hepatocyte ATF3 in NAFLD

NIH RePORTER · NIH · R01 · $458,214 · view on reporter.nih.gov ↗

Abstract

Project Summary Project Summary: Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in developed countries, which ranges from simple steatosis to non-alcoholic steatohepatitis (NASH). So far, the mechanisms underlying the development of NAFLD is poorly understood. Activating transcription factor 3 (ATF3) is a member of the ATF/cAMP response element-binding (ATF/CREB) family of transcription factors, and inhibits inflammatory response in macrophages. Until now, nothing has been known about the role of hepatic ATF3 in lipid metabolism. Our preliminary studies have shown that hepatic ATF3 expression is markedly reduced under common metabolic stress. Over-expression of ATF3 in the liver improves lipid homeostasis whereas loss of hepatic ATF3 has opposite effects. In this project, we will investigate whether and how hepatic ATF3 regulates the development of NAFLD. We will use both gain- and loss-of-function approaches to complete this project. Completion of the proposed studies may help identify hepatocyte ATF3 as a key regulator of lipid metabolism and the development of NAFLD.

Key facts

NIH application ID
10224182
Project number
5R01DK118941-04
Recipient
NORTHEAST OHIO MEDICAL UNIVERSITY
Principal Investigator
Yanqiao Zhang
Activity code
R01
Funding institute
NIH
Fiscal year
2021
Award amount
$458,214
Award type
5
Project period
2018-08-01 → 2024-03-31