Commentary
Progress in uncovering pathogenic determinants of fibrosis in NASH include metabolic dysregulation in hepatocytes that induce inflammation and cytokine secretion leading to cell injury and apoptosis, among others.
This review by T. M. Huisman et al. (Division of Liver Diseases, Icahn School of Medicine at Mount Sinai, New York, USA) highlights key experimental and investigational therapies for NASH fibrosis, whose evaluation will be accelerated as new non-invasive markers of fibrosis are established.
There is growing optimism that new pharmacotherapies are likely to emerge within the next 3 years that will favourably alter the natural history of disease. Along these “targeted therapies”, lanifibranor, an indole sulfonamide PPAR agonist, activates the three subtypes α, δ and γ. Due to its mechanism of action, lanifibranor addresses all the key features of NASH: inflammation, steatosis, ballooning, and – importantly – fibrosis.
