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The L\u2010\u03b1\u2010lysophosphatidylinositol\/G protein\u2010coupled receptor 55 (LPI\/GPR55) axis, an element of the endocannabinoidome, has emerged as a key driver behind liver disease progression, leading to the progression of metabolic dysfunction associated steatohepatitis (MASH). Implicated in hepatic lipid accumulation, inflammation and fibrosis, this axis has detrimental effects in hepatocytes, Kupffer cells and hepatic stellate cells. Furthermore, recent evidence suggests that this axis induces\n                    <jats:italic>de novo<\/jats:italic>\n                    lipogenesis, promoting pro\u2010inflammatory cytokine production, leading to fibrosis and the transition toward a steatotic liver. The enzyme membrane\u2010bound O\u2010acyltransferase domain\u2010containing 7 (MBOAT7) modulates this axis by acylation of LPI, exacerbating hepatic steatosis and insulin resistance. Until recently, no pharmacologic treatments were approved for MAFLD. However, resmetirom received FDA approval in March 2024 for the treatment of MASH, and semaglutide (Wegovy) was granted accelerated FDA approval in August 2025 for MASH with moderate\u2010to\u2010advanced fibrosis. Additional agents such as tirzepatide and retatrutide remain in late\u2010stage clinical development. We propose that targeting the endocannabinoidome, specifically the LPI\/GPR55 axis, represents a promising therapeutic strategy for liver disease. Previous attempts to target GPR55 therapeutically have involved small\u2010molecule agonists and phytocannabinoids with antagonistic activity. However, progress remains limited due to the context\u2010specific roles of GPR55 across different tissues and signalling pathways. As such, future strategies involving the LPI\/GPR55 axis must focus on hepatic\u2010specific GPR55 modulation using selective ligands and advanced delivery systems, mitigating off\u2010target effects. This review elucidates the mechanistic role of the LPI\/GPR55 axis, combining the role of MBOAT7 in the pathophysiology of metabolic\u2010associated liver disease.\n                  <\/jats:p>","DOI":"10.1111\/liv.70576","type":"journal-article","created":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T09:41:25Z","timestamp":1773394885000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Targeting the\n                    <scp>LPI<\/scp>\n                    \/\n                    <scp>GPR55<\/scp>\n                    Axis in\n                    <scp>MAFLD<\/scp>\n                    and\n                    <scp>MASH<\/scp>\n                    : Novel Insights, Therapeutic Strategies and Future 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