Single, dual and pan-PPAR agonists are under development for the pharmacological treatment of NASH, ? read more from our articles.
Recent technological advancements have provided unprecedented insights into the inflammatory mechanisms underlying liver fibrosis, leading to the identification of promising novel targets for anti-inflammatory and antifibrotic therapies.
Peroxisome proliferated-activated receptors (PPARs), including α, β/δ and γ isotypes, are a nuclear receptor family of lipid sensors activated by natural fatty acid derivatives and pharmacological agonists.
Non-alcoholic fatty liver disease (NAFLD) can be categorised into two disease sub-classifications: non-alcoholic fatty liver (NAFL), its non-progressive subtype, and non-alcoholic steatohepatitis (NASH), its progressive form.
Non-alcoholic steatohepatitis (NASH) is characterised by complex interactions between intricate intra- and extra-hepatic drivers, encompassing numerous metabolic, inflammatory, vascular, and fibrogenic pathways.
Categories: PPAR Articles, NASH Biomarker, Pathophysiology Articles, Management Articles
The last decade has seen an unprecedented amount of data in the way of therapeutic research for non-alcoholic steatohepatitis (NASH), the progressive form of non-alcoholic fatty liver disease (NAFLD).
Generally, NASH and fibrosis correlate with the development of cirrhosis and other negative clinical outcomes. Treatments often aim to target inflammation, fibrosis, cell injury or metabolic dysregulation.
Although it is known that non-alcoholic steatohepatitis (NASH) increases the risk of end-stage liver diseases such as cirrhosis and hepatocellular carcinoma, no pharmacologic therapy has yet been approved to treat it.