Druggable genome-wide Mendelian randomization identifies therapeutic targets for metabolic dysfunction-associated steatotic liver disease

Abstract Background Metabolic dysfunction-associated steatotic liver disease (MASLD) affects > 25% of the global population, potentially leading to severe hepatic and extrahepatic complications, including metabolic dysfunction-associated steatohepatitis. Given that the pathophysiology of MASLD is...

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Main Authors: Xiaohui Ma, Li Ding, Shuo Li, Yu Fan, Xin Wang, Yitong Han, Hengjie Yuan, Longhao Sun, Qing He, Ming Liu
Format: Article
Language:English
Published: BMC 2025-03-01
Series:Lipids in Health and Disease
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Online Access:https://doi.org/10.1186/s12944-025-02515-8
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author Xiaohui Ma
Li Ding
Shuo Li
Yu Fan
Xin Wang
Yitong Han
Hengjie Yuan
Longhao Sun
Qing He
Ming Liu
author_facet Xiaohui Ma
Li Ding
Shuo Li
Yu Fan
Xin Wang
Yitong Han
Hengjie Yuan
Longhao Sun
Qing He
Ming Liu
author_sort Xiaohui Ma
collection DOAJ
description Abstract Background Metabolic dysfunction-associated steatotic liver disease (MASLD) affects > 25% of the global population, potentially leading to severe hepatic and extrahepatic complications, including metabolic dysfunction-associated steatohepatitis. Given that the pathophysiology of MASLD is incompletely understood, identifying therapeutic targets and optimizing treatment strategies are crucial for addressing this severe condition. Methods Mendelian randomization (MR) analysis was conducted using two genome-wide association study datasets: a European meta-analysis (8,434 cases; 770,180 controls) and an additional study (3,954 cases; 355,942 controls), identifying therapeutic targets for MASLD. Of 4302 drug-target genes, 2,664 genetic instrument variables were derived from cis-expression quantitative trait loci (cis-eQTLs). Colocalization analyses assessed shared causal variants between MASLD-associated single nucleotide polymorphisms and eQTLs. Using the drug target gene cis-eQTL of liver tissue from the genotype-tissue expression project, we performed MR and summary MR to validate the significance of the gene results of the blood eQTL MR. RNA-sequencing data from liver biopsies were validated using immunohistochemistry and quantitative polymerase chain reaction (qPCR) tests to confirm gene expression findings. Result MR analysis across both datasets identified significant MR associations between MASLD and two drug targets—milk fat globule-EGF factor 8 (MFGE8) (odds ratio [OR] 0.89, 95% confidence interval [CI] 0.85–0.94; P = 2.15 × 10−6) and cluster of differentiation 33 (CD33) (OR 1.17, 95% CI 1.10–1.25; P = 1.39 × 10−6). Both targets exhibited strong colocalization with MASLD. Genetic manipulation indicating MFGE8 activation and CD33 inhibition did not increase the risk for other metabolic disorders. RNA-sequencing, qPCR, and immunohistochemistry validation demonstrated consistent differential expressions of MFGE8 and CD33 in MASLD. Conclusion CD33 inhibition can reduce MASLD risk, while MFGE8 activation may offer therapeutic benefits for MASLD treatment.
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spelling doaj-art-1e77d6ad323945e8a39909d9bcc0ada92025-08-20T02:10:21ZengBMCLipids in Health and Disease1476-511X2025-03-0124111510.1186/s12944-025-02515-8Druggable genome-wide Mendelian randomization identifies therapeutic targets for metabolic dysfunction-associated steatotic liver diseaseXiaohui Ma0Li Ding1Shuo Li2Yu Fan3Xin Wang4Yitong Han5Hengjie Yuan6Longhao Sun7Qing He8Ming Liu9Department of Endocrinology and Metabolism, Tianjin Medical University General HospitalDepartment of Endocrinology and Metabolism, Tianjin Medical University General HospitalDepartment of Endocrinology and Metabolism, Tianjin Medical University General HospitalDepartment of Endocrinology and Metabolism, Tianjin Medical University General HospitalDepartment of Endocrinology and Metabolism, Tianjin Medical University General HospitalDepartment of General Surgery, Tianjin Medical University General HospitalDepartment of Pharmacy, Tianjin Medical University General HospitalDepartment of General Surgery, Tianjin Medical University General HospitalDepartment of Endocrinology and Metabolism, Tianjin Medical University General HospitalDepartment of Endocrinology and Metabolism, Tianjin Medical University General HospitalAbstract Background Metabolic dysfunction-associated steatotic liver disease (MASLD) affects > 25% of the global population, potentially leading to severe hepatic and extrahepatic complications, including metabolic dysfunction-associated steatohepatitis. Given that the pathophysiology of MASLD is incompletely understood, identifying therapeutic targets and optimizing treatment strategies are crucial for addressing this severe condition. Methods Mendelian randomization (MR) analysis was conducted using two genome-wide association study datasets: a European meta-analysis (8,434 cases; 770,180 controls) and an additional study (3,954 cases; 355,942 controls), identifying therapeutic targets for MASLD. Of 4302 drug-target genes, 2,664 genetic instrument variables were derived from cis-expression quantitative trait loci (cis-eQTLs). Colocalization analyses assessed shared causal variants between MASLD-associated single nucleotide polymorphisms and eQTLs. Using the drug target gene cis-eQTL of liver tissue from the genotype-tissue expression project, we performed MR and summary MR to validate the significance of the gene results of the blood eQTL MR. RNA-sequencing data from liver biopsies were validated using immunohistochemistry and quantitative polymerase chain reaction (qPCR) tests to confirm gene expression findings. Result MR analysis across both datasets identified significant MR associations between MASLD and two drug targets—milk fat globule-EGF factor 8 (MFGE8) (odds ratio [OR] 0.89, 95% confidence interval [CI] 0.85–0.94; P = 2.15 × 10−6) and cluster of differentiation 33 (CD33) (OR 1.17, 95% CI 1.10–1.25; P = 1.39 × 10−6). Both targets exhibited strong colocalization with MASLD. Genetic manipulation indicating MFGE8 activation and CD33 inhibition did not increase the risk for other metabolic disorders. RNA-sequencing, qPCR, and immunohistochemistry validation demonstrated consistent differential expressions of MFGE8 and CD33 in MASLD. Conclusion CD33 inhibition can reduce MASLD risk, while MFGE8 activation may offer therapeutic benefits for MASLD treatment.https://doi.org/10.1186/s12944-025-02515-8CD33Mendelian randomization analysisMFGE8Non-alcoholic fatty liver diseaseNonalcoholic steatohepatitis
spellingShingle Xiaohui Ma
Li Ding
Shuo Li
Yu Fan
Xin Wang
Yitong Han
Hengjie Yuan
Longhao Sun
Qing He
Ming Liu
Druggable genome-wide Mendelian randomization identifies therapeutic targets for metabolic dysfunction-associated steatotic liver disease
Lipids in Health and Disease
CD33
Mendelian randomization analysis
MFGE8
Non-alcoholic fatty liver disease
Nonalcoholic steatohepatitis
title Druggable genome-wide Mendelian randomization identifies therapeutic targets for metabolic dysfunction-associated steatotic liver disease
title_full Druggable genome-wide Mendelian randomization identifies therapeutic targets for metabolic dysfunction-associated steatotic liver disease
title_fullStr Druggable genome-wide Mendelian randomization identifies therapeutic targets for metabolic dysfunction-associated steatotic liver disease
title_full_unstemmed Druggable genome-wide Mendelian randomization identifies therapeutic targets for metabolic dysfunction-associated steatotic liver disease
title_short Druggable genome-wide Mendelian randomization identifies therapeutic targets for metabolic dysfunction-associated steatotic liver disease
title_sort druggable genome wide mendelian randomization identifies therapeutic targets for metabolic dysfunction associated steatotic liver disease
topic CD33
Mendelian randomization analysis
MFGE8
Non-alcoholic fatty liver disease
Nonalcoholic steatohepatitis
url https://doi.org/10.1186/s12944-025-02515-8
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