ArticleHepatology communications2024
Liver-specific mitochondrial amidoxime-reducing component 1 (Mtarc1) knockdown protects the liver from diet-induced MASH in multiple mouse models.
Article in Hepatology communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Prime editing models the MTARC1 A165T variant in human liver organoids, demonstrating reduced steatosis, inflammation, and fibrosis.Hepatology communications · 2026Article
- Divergence of the CYB5R3-mARC1 Redox Axis Across the Human MASLD-to-Hepatocellular-Carcinoma Continuum: An Exploratory Analysis of Liver-Biopsy and Tumor Cohorts.International journal of molecular sciences · 2026Article
- Integrating CRISPR genome editing with liver organoid and hiPSC-derived microfluidic platforms to model metabolic dysfunction-associated steatotic liver disease.Biochemistry and biophysics reports · 2026Review
- Metabolic dysfunction-associated steatotic liver disease: pathogenesis and novel treatment options.Molecular biomedicine · 2026Review
- Sex- and mouse strain-related differences in body weight gain, composition of the gut microbiota, and levels of selected metabolites in response to a Western-style diet.BMC gastroenterology · 2026Article
- Loss of Mtarc1 Protects Against Steatotic Liver Disease in Mice.Liver international : official journal of the International Association for the Study of the Liver · 2026Article
- A mitochondrial amidoxime-reducing component 1 (mARC1) A168T amino acid substitution does not confer protection from MASH and fibrosis in multiple mouse models of chronic liver disease.The Biochemical journal · 2026Article
- MASLD/MASH-New mechanisms and treatments.Hepatology communications · 2025Article
- Polymorphism's MBOAT7 as Risk and MTARC1 as Protection for Liver Fibrosis in MASLD.International journal of molecular sciences · 2025Article
- Gene-based therapies for steatotic liver disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- Hepatic HSD17B6 is dispensable for diet-induced fatty liver disease in mice.Biochemistry and biophysics reports · 2025Article
- Precision medicine and nucleotide-based therapeutics to treat steatotic liver disease.Clinical and molecular hepatology · 2025Review
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15 authors.
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Abstract
backgroundHuman genetic studies have identified several mitochondrial amidoxime-reducing component 1 (MTARC1) variants as protective against metabolic dysfunction-associated steatotic liver disease. The MTARC1 variants are associated with decreased plasma lipids and liver enzymes and reduced liver-related mortality. However, the role of mARC1 in fatty liver disease is still unclear.
methodsGiven that mARC1 is mainly expressed in hepatocytes, we developed an N-acetylgalactosamine-conjugated mouse Mtarc1 siRNA, applying it in multiple in vivo models to investigate the role of mARC1 using multiomic techniques.
resultsIn ob/ob mice, knockdown of Mtarc1 in mouse hepatocytes resulted in decreased serum liver enzymes, LDL-cholesterol, and liver triglycerides. Reduction of mARC1 also reduced liver weight, improved lipid profiles, and attenuated liver pathological changes in 2 diet-induced metabolic dysfunction-associated steatohepatitis mouse models. A comprehensive analysis of mARC1-deficient liver from a metabolic dysfunction-associated steatohepatitis mouse model by metabolomics, proteomics, and lipidomics showed that Mtarc1 knockdown partially restored metabolites and lipids altered by diet.
conclusionsTaken together, reducing mARC1 expression in hepatocytes protects against metabolic dysfunction-associated steatohepatitis in multiple murine models, suggesting a potential therapeutic approach for this chronic liver disease.
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