Peter J. Havel

Deletion of protein tyrosine phosphatase 1B in hepatocytes attenuates inflammation, steatosis, and fibrosis in a dietary mouse model of metabolic dysfunction-associated steatohepatitis

Abstract Background Metabolic dysfunction-associated steatohepatitis (MASH) is a leading cause of liver-related morbidity and mortality. The current interventions are limited, underscoring the need for novel mechanism-based therapies. Protein tyrosine phosphatase 1B (PTP1B) regul...