ReviewNature reviews. Gastroenterology & hepatology2026
Germline mutations and somatic mosaicism in steatotic liver diseases and related liver carcinogenesis.
Review in Nature reviews. Gastroenterology & hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Authors and funding
3 authors.
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Abstract
Steatotic liver diseases, encompassing metabolic dysfunction-associated steatotic liver disease and alcohol-related liver disease, affect nearly one-third of the global population and are a leading cause of cirrhosis and hepatocellular carcinoma. The substantial interindividual variation in disease progression indicates important genetic contributions beyond environmental factors. Genome-wide association studies have identified multiple common variants predominantly affecting lipid metabolism, with PNPLA3 I148M representing the strongest genetic determinant across the disease spectrum. The shared genetic architecture across metabolic dysfunction-associated steatotic liver disease and alcohol-related liver disease supports convergent pathogenic mechanisms. Discoveries of somatic mosaicism in adult liver tissues have revealed convergent mutations in metabolic genes such as FOXO1, GPAM and CIDEB, conferring adaptive advantages against lipotoxicity. Also, clonal haematopoiesis of indeterminate potential is associated with the risk of chronic liver diseases, metabolic dysfunction-associated steatohepatitis and its related liver cancer risk. Inherited and somatic variants can influence hepatocellular carcinoma risk through direct effects on chronic liver disease progression and/or through specific cancer-promoting pathways involving telomere maintenance and WNT signalling. Although polygenic risk scores represent a promising approach for risk stratification, current implementations face important limitations that must be addressed before achieving their full clinical potential.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.