Impact of platelet phenotype on liver fibrosis progression in metabolic dysfunction-associated steatotic liver disease

During the last decades, lifestyle changes have deeply influenced human metabolism, giving rise to a global silent epidemic of chronic metabolic diseases worldwide, encompassing obesity, type 2 diabetes (T2D), and non-alcoholic fatty liver disease (NAFLD). NAFLD, now referred to as metabolic dysfunction-associated steatotic liver disease (MASLD), has become the most common cause of chronic liver disease. Robust scientific evidence closely links it with metabolic syndrome features, especially obesity and type 2 diabetes. MASLD results from the accumulation of liver fat, occurring in the absence of significant alcohol consumption and within the context of at least one metabolic dysfunction. This condition encompasses a spectrum of histopathological changes from simple steatosis (metabolic dysfunction-associated steatotic liver, MASL) to steatohepatitis (metabolic dysfunction-associated steatohepatitis, MASH) and may further lead to significant fibrosis and, eventually, MASH-related cirrhosis. The progression of MASL to MASH is not fully elucidated. While platelets have a well-established role in hemostasis, recent studies have revealed their active involvement in the inflammatory response and tissue remodeling. However, their role in MASLD progression remains unclear and subject to ongoing debate. This study aims to identify specific features of platelet phenotype across different stages of MASLD and to explore potential biomarkers linked to platelet phenotype that may predict significant fibrosis in affected patients.