Novel intervention for alcohol-associated liver disease

Abstract

A recently published article in the World Journal of Gastroenterology clarified that elafibranor, a dual peroxisome proliferator activated receptor α/δ (PPARα/δ) agonist, reduced inflammation and fibrosis in alcohol-associated liver disease (ALD). This letter aims to discuss the findings presented in that article. ALD is a global health problem, and no effective drugs has been approved by the Food and Drug Administration to cure it. Thus, finding targeted therapies is of great urgency. Herein, we focus on the pathogenesis of ALD and the role of PPARα/δ in its development. Consistent with the conclusion of the article of interest, we think that elafibranor may be a promising therapeutic option for ALD, due to the pivotal involvement of PPARα/δ in the pathogenesis of the disease. However, its treatment dose, timing, and side effects need to be further investigated in future studies.

Keywords: Alcohol-associated liver disease; Elafibranor; Pathogenesis; Peroxisome proliferator activated receptor α/δ; Therapy.

Figure 1

Pathogeneses of alcohol-associated liver disease. The primary mechanisms involved in the development of alcohol-associated liver disease are listed. Cell death and regeneration, inflammation, the gut-liver axis, lipid metabolism, and mitochondrial dysfunction all contribute to the development of alcohol-associated liver disease. Created with BioRender.com. TNF-α: Tumor necrosis factor-α; IL: Interleukin; TGF-β: Transforming growth factor-β.