Non-alcoholic steatohepatitis articles from across Nature Portfolio

Current drug approvals reshape metabolic dysfunction-associated steatohepatitis (MASH) therapeutic strategies. This Review highlights current and emerging therapeutic targets and discusses a mechanism-based framework for personalized, combination-oriented management in MASH.

SLCO4C1 is known for regulating kidney diseases. This study showed SLCO4C1 regulates hepatic cAMP uptake to suppress lipogenesis in MASLD. Targeting this pathway by FGF21 or forskolin suppressed lipogenesis.

Hepatocyte-specific GPR110 mediates metabolic dysfunction-associated steatohepatitis progression by regulating hepatic oestrogen sensitivity in a sex-specific manner, specifically in female mice.

Nicotine exacerbates MASH by disrupting gut microbiota and impairing intestinal barrier integrity via HIF-1α suppression, while probiotic supplementation mitigates nicotine-induced liver injury

Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as the most common chronic liver disease worldwide, with the Middle East and North Africa (MENA) being severely affected. By shifting towards preventive hepatology, MENA can mitigate the rising tide of MASLD and its complications, reduce health system costs and improve patient outcomes.

A proteomic study begins to identify the direct and indirect effects of GLP-1 treatment on metabolic dysfunction-associated steatohepatitis (MASH), and reveals insights into treatment-induced changes in liver histology.