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Article

Prime editing models the MTARC1 A165T variant in human liver organoids, demonstrating reduced steatosis, inflammation, and fibrosis.

Hepatology communications - 1 Oct 2026

Ben Saad Amel, Arghiani Nahid, Weilheimer Arden D, Gentile Stefan D, Toles Benjamin J, Tripathi Sudipta, Mohsin Sayed Seher, Chandraker Anil, Mullen Alan C

Abstract excerpt

BACKGROUND: Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent cause of chronic liver disease worldwide. This progressive, multifactorial condition is characterized by hepatic steatosis, which can evolve into steatohepatitis, fibrosis, cirrhosis, and liver cancer. Genetic factors influence the development, progression, and complications in MASLD, and genome-wide association...

Read the complete abstract on PubMed

Topics

Humans
Liver
Liver Cirrhosis
Polymorphism, Single Nucleotide
Organoids
Fatty Liver

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Oxidoreductases

Human Embryonic Stem Cells

Hepatocytes

Source

Open in PubMed Open full text

Identifiers

PMID: 42748411
DOI: 10.1097/HC9.0000000000001022
PMCID: PMC13585322

Genes

MTARC1
THRB

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 21 Oct 2026.

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Prime editing models the MTARC1 A165T variant in human liver organoids, demonstrating reduced steatosis, inflammation, and fibrosis.PMID 42748411Read ↗

Prime Editing Models the MTARC1 A165T Variant in Human Liver Organoids, Demonstrating Reduced Steatosis, Inflammation, and FibrosisSemantic proximity Read ↗

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