LAUSR

In parallel to the obesity pandemic, nonalcoholic fatty liver disease (NAFLD) has become the most common cause of chronic liver disease in adults worldwide [1]. Especially its inflammatory form, nonalcoholic steatohepatitis (NASH), but ‘simple steatosis’ as well, can progress to fibrosis, cirrhosis and hepatocellular carcinoma. In these patients, the degree of liver fibrosis is the main histological predictor of liver-related and overall mortality [2]. Although this is an area of intense investigation, there is currently no approved pharmacotherapy for NAFLD. Whereas most compounds intend to correct aberrant metabolism by targeting insulin resistance and hepatic fat accumulation, chemokine (receptor) inhibitors act on inflammatory pathways with the ultimate aim to attenuate, or even reverse, scar tissue formation [3]. In this regard, inhibitors of either C-C chemokine receptors (CCR) 2 and 5 or their respective ligands are of interest for treating NAFLD. CCR2/5 inhibitors have proven to be effective in reducing fibrosis in animal models of NASH and fibrosis through targeting disease-promoting liver macrophages and hepatic stellate cells and have advanced to clinical trials.