Abstract
<jats:p>Metabolic dysfunction – Associated Steatotic Liver Disease (MASLD) represents the emerging leading cause of Chronic Liver Disease (CLD) worldwide, with a global prevalence of approx. 30% in the general population that parallels global rates of obesity and Type 2 Diabetes (T2D). At present no validated therapy is available to block or slow down disease progression to Metabolic dysfunction – Associated SteatoHepatitis (MASH), liver fibrosis and cirrhosis and hepatocellular carcinoma (HCC). At present there is a lack of reliable biomarkers able to identify MASH patients at risk of disease progression and/or HCC development. According to the knowledge that pro-inflammatory cytokines play a key role in MASLD/MASH progression and HCC development, in this review we will discuss the role in this disease and other CLD of Oncostatin M (OSM), a cytokine belonging to the IL-6 family, and of pathways involving OSM and its receptor β (OSM/OSMRβ axis). OSM and related pathways are emerging as selective in sustaining disease progression by promoting chronic inflammation and fibrogenesis. Moreover, OSM/OSMRβ axis is critically involved in MASH-related HCC development by affecting proliferation, angiogenesis, invasiveness and metastasis as well as by reshaping MASH-related tumour immune microenvironment. OSM/OSMRβ axis is then emerging as a selective MASH-related putative therapeutic target.</jats:p>