Semin Liver Dis 2019; 39(03): 291-300
DOI: 10.1055/s-0039-1687851
Review Article
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Macrophages as Key Players during Adipose Tissue–Liver Crosstalk in Nonalcoholic Fatty Liver Disease

Hannelie Korf
1  Laboratory of Hepatology, CHROMETA Department, KU Leuven, Leuven, Belgium
,
Markus Boesch
1  Laboratory of Hepatology, CHROMETA Department, KU Leuven, Leuven, Belgium
,
Lore Meelberghs
1  Laboratory of Hepatology, CHROMETA Department, KU Leuven, Leuven, Belgium
,
Schalk van der Merwe
1  Laboratory of Hepatology, CHROMETA Department, KU Leuven, Leuven, Belgium
2  Department of Gastroenterology and Hepatology, UZ Leuven, Leuven, Belgium
› Author Affiliations
Further Information

Publication History

Publication Date:
30 April 2019 (eFirst)

Abstract

Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in Western countries that could lead to serious health problems including liver failure, cancer, or death. The term NAFLD includes a spectrum of disease states with histological features ranging from simple steatosis to nonalcoholic steatohepatitis (NASH). A key aspect within this research field is the identification of pathogenic factors that trigger inflammation, thus fueling the transition from nonalcoholic fatty liver to NASH. These inflammatory triggers may originate from within the liver as a result of innate immune cell activation and/or hepatocyte injury. Additionally, they may originate from other sites such as adipose tissue or the intestinal tract. In the current review, the authors will primarily focus on events within adipose tissue which may be of importance in triggering the disease progression. They specifically focus on the role of adipose tissue macrophages during NAFLD pathogenesis and how microenvironmental factors may shape their metabolic profile. They further dissect how redirecting the macrophage's metabolic profile alters their immunological functions. Finally, they discuss the opportunities and challenges of targeting macrophages to interfere in disease progression.