Introduction: Metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH) are now recognized as systemic metabolic diseases rather than isolated liver disorders. This review integrates current knowledge on how hormonal, metabolic, inflammatory, and fibrotic pathways interact to drive disease progression.
Introduction:
Metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH) are now recognized as systemic metabolic diseases rather than isolated liver disorders. This review integrates current knowledge on how hormonal, metabolic, inflammatory, and fibrotic pathways interact to drive disease progression.
Why was this review needed?
Despite major advances in understanding MASLD, the mechanisms linking obesity, insulin resistance, adipose dysfunction, and chronic inflammation to progressive liver fibrosis remain incompletely integrated. A comprehensive understanding is essential for developing precision therapies.
What did the review show?
Clinical Impact:
MASLD should be managed as a multisystem metabolic disease rather than a liver-specific disorder. Targeting insulin resistance, adipose dysfunction, hormonal imbalance, and chronic inflammation may help prevent progression to MASH and advanced fibrosis.
Take-Home Message:
MASLD and MASH result from complex interactions between metabolic dysfunction, hormonal imbalance, inflammation, and fibrosis. Understanding these interconnected pathways provides the foundation for precision medicine and the development of mechanism-based therapies that target disease progression rather than hepatic steatosis alone.
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Introduction: Metabolic dysfunction-associated steatohepatitis (MASH) remains a leading cause of cirrhosis, liver failure, and hepatocellular carcinoma, with limited treatment options. This study evaluated DT-109, a novel glycine-based tripeptide, as a gut-targeted therapy aimed at restoring...
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