Targeting the LPI/GPR55 Axis in MAFLD and MASH: Novel Insights, Therapeutic Strategies and Future Directions.

Journal	Liver international : official journal of the International Association for the Study of the Liver
Study Type	Clinical Study
Population	Human participants

This research identifies a specific cannabinoid-related pathway (LPI/GPR55) that drives progression from fatty liver to more severe inflammatory liver disease. Understanding this mechanism could lead to targeted interventions for the millions of patients with metabolic liver disease.

This clinical study examined the L-α-lysophosphatidylinositol/GPR55 receptor axis, part of the broader endocannabinoid system, in human participants with metabolic dysfunction-associated fatty liver disease (MAFLD). The research demonstrates that this pathway promotes harmful liver changes including fat accumulation, inflammation, and scarring across multiple liver cell types. The study also identified that the enzyme MBOAT7 worsens disease progression by modifying this pathway, leading to increased liver fat storage and insulin resistance.

“While this advances our understanding of how endocannabinoid-related pathways contribute to liver disease, it doesn’t immediately change my clinical approach. The therapeutic implications remain theoretical until we have interventional data.”

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