Non-alcoholic fatty liver disease (NAFLD) has a more progressive form, non-alcoholic steatohepatitis (NASH). In both conditions, inflammation is a key driver of the pathogenesis. There are various causes of metabolic injury in the conditions, leading to the activation of different immune cells such as hepatic Kupffer cells. In turn, these activate other immune cells through the release of inflammatory cytokines. This causes inflammation to progress.
Targeting inflammation in NAFLD and NASH has been attempted through inhibiting immune cell recruitment, through methods such as chemokine receptors or the neutralisation of CD44. Secretion of regenerative growth factors, anti-inflammatory cytokines and the use of neutrophils has also been tried to resolve inflammation. Some of these therapies will be attempted to be used as a personalised combination therapy, as there is currently no specific treatment for this condition. Generally, the approach is to inhibit immune cells activation and recruitment. CCR2/5 antagonists and antifibrotic therapies are largely being investigated to this end.
This review by Wiering L & Tacke F aimed to understand the importance of inflammation and anti-inflammatory therapies for NAFLD and NASH.
NAFLD and NASH are complex pathologies, with inflammation being a key part of the disease. Inhibiting inflammatory pathways or reversing inflammation may hold the key to a future therapy. However, the question of which specific cells or pathways need to be targeted is not yet fully researched.