Role of histone deacetylase on nonalcoholic fatty liver disease

ABSTRACT

Introduction

Nonalcoholic fatty liver disease (NAFLD) is a group of diseases related to metabolic abnormalities, which severely impairs the life and health of patients, and brings great pressure to the society and medical resources. Currently, there is no specific treatment. Histone deacetylases (HDACs) have recently been reported to be involved in the pathogenesis of NAFLD and are considered as new targets for the treatment of NAFLD.

Area covered

In this review, we summarized the role of HDACs in the pathogenesis of NAFLD and proposed possible therapeutic targets in order to provide new strategies for the treatment of NAFLD.

Expert commentary

HDACs and related signal pathways are widely involved in the pathogenesis of NAFLD and have the potential to become therapeutic targets. However, based on current research alone, HDACs cannot be practical applied to the treatment of NAFLD. Therefore, more research on the pathogenesis of NAFLD and the mechanism of HDACs is what we need most now.

KEYWORDS:

• Nonalcoholic fatty liver disease
• histone deacetylases
• sirtuins
• therapeutic targets
• deacetylation

Article highlights

• HDACs are involved in the pathogenesis of NAFLD. Different types of HDACs participate in different signaling pathways, and their effects are also different.

• Reported HDACs that may improve NAFLD are: HDAC1, 2, 3, and SIRT1. The HDACs that may promote NAFLD are: HDAC7, 8, and 11. HDACs that are still controversial about the role of NAFLD are: HDAC6 and SIRT3. The remaining HDACs are still lack of relevant research.

• The practical application of HDACs to the treatment of NAFLD requires more research support. In-depth exploration of the pathogenesis of NAFLD and the mechanism of action of HDACs will promote this process.

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grant or patents received or pending, or royalties.

Reviewer Disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper was not funded.