Protective hepatocyte signals restrain liver fibrosis in metabolic dysfunction-associated steatohepatitis.

Steffani, Marcella; Geng, Yana; Pajvani, Utpal B; Schwabe, Robert F

Steffani, Marcella; Geng, Yana; Pajvani, Utpal B; Schwabe, Robert F.

Afiliación

Steffani M; Department of Medicine, Columbia University, New York, New York, USA.
Geng Y; Department of Medicine, Columbia University, New York, New York, USA.
Pajvani UB; Department of Medicine, Columbia University, New York, New York, USA.
Schwabe RF; Institute of Human Nutrition, New York, New York, USA.

J Clin Invest ; 134(7)2024 Apr 01.

Article en En | MEDLINE | ID: mdl-38557494

ABSTRACT

ABSTRACT

Metabolic dysfunction-associated steatotic liver disease (MASLD) affects nearly 40% of the global adult population and may progress to metabolic dysfunction-associated steatohepatitis (MASH), and MASH-associated liver fibrosis and cirrhosis. Despite numerous studies unraveling the mechanism of hepatic fibrogenesis, there are still no approved antifibrotic therapies. The development of MASLD and liver fibrosis results from complex cell-cell interactions that often initiate within hepatocytes but remain incompletely understood. In this issue of the JCI, Yan and colleagues describe an ATF3/HES1/CEBPA/OPN pathway that links hepatocyte signals to fibrogenic activation of hepatic stellate cells and may provide new perspectives on therapeutic options for MASLD-induced liver fibrosis.

Asunto(s)

Hígado Graso; Cirrosis Hepática; Adulto; Humanos; Hepatocitos; Células Estrelladas Hepáticas; Comunicación Celular

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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Hígado Graso / Cirrosis Hepática Límite: Adult / Humans Idioma: En Revista: J Clin Invest Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos

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