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To narrow the translational gap in the development of pharmacological MASH treatments, a 3D liver model\u00a0from primary human hepatocytes and non\u2010parenchymal cells derived from patients with histologically confirmed MASH was established. The model closely mirrors disease\u2010relevant endpoints, such as steatosis, inflammation and fibrosis, and multi\u2010omics analyses show excellent alignment with biopsy data from 306 MASH patients and 77 controls. By combining high\u2010content imaging with scalable biochemical assays and chemogenomic screening, multiple novel targets with anti\u2010steatotic, anti\u2010inflammatory, and anti\u2010fibrotic effects are identified. Among these, activation of the muscarinic M<jats:sub>1<\/jats:sub> receptor (CHRM1) and inhibition of the TRPM8 cation channel result in strong anti\u2010fibrotic effects, which are confirmed using orthogonal genetic assays. Strikingly, using biosensors based on bioluminescence resonance energy transfer, a functional interaction along a novel MASH signaling axis in which CHRM1 inhibits TRPM8 via G<jats:sub>q\/11<\/jats:sub> and phospholipase C\u2010mediated depletion of phosphatidylinositol 4,5\u2010bisphosphate can be demonstrated. 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