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Metabolic dysfunction-associated steatotic liver disease (MASLD) and its inflammatory progression to metabolic dysfunction-associated steatohepatitis (MASH) represent a major global health burden with a complex, multifactorial pathogenesis.1 While hepatic steatosis remains a defining feature of MASLD, disease progression to steatohepatitis and fibrosis reflects the interplay of multiple pathogenic processes. Among these, gut–liver axis dysfunction, characterised by intestinal dysbiosis, dysregulated microbial metabolism and impaired barrier integrity, has emerged as a key contributor.