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Optimized Analysis of In Vivo and In Vitro Hepatic Steatosis
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Genome Editing and Fatty Liver.

Umar Hayat1, Ali A Siddiqui2, Muhammad L Farhan3

  • 1Department of Population and Public Health, University of Kansas, Wichita, KS, USA. umarhayat216@gmail.com.

Advances in Experimental Medicine and Biology
|December 1, 2022
PubMed
Summary
This summary is machine-generated.

Fatty liver disease, including NAFLD and ALD, involves excessive liver fat accumulation with complex genetic causes. This review explores gene variants and advanced CRISPR/Cas9 genome editing models for developing new fatty liver disease treatments.

Keywords:
Alcoholic liver disease (ALD)Clustered regularly interspaced short palindromic repeats (CRISPR/Cas9)Fatty liver diseaseGenome editingNonalcoholic fatty liver disease (NAFLD)

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Area of Science:

  • Hepatology and Genetics
  • Molecular Biology and Disease Mechanisms

Background:

  • Fatty liver disease, encompassing nonalcoholic fatty liver disease (NAFLD) and alcoholic liver disease (ALD), is a prevalent global health issue characterized by hepatic lipid accumulation.
  • It presents a genetically diverse etiology, complex pathogenesis, and significant contributions to morbidity, mortality, and healthcare expenditures.
  • Risk factors for NAFLD include metabolic syndrome, obesity, type 2 diabetes, and dyslipidemia, while ALD is linked to excessive alcohol consumption.

Approach:

  • This review details the roles of specific gene variants and their encoded proteins in the pathogenesis of NAFLD and ALD.
  • It examines the application of advanced genome engineering technologies, particularly clustered regularly interspaced short palindromic repeats (CRISPR/Cas9) and its variants (prime and base editors), in creating in vivo and in vitro models of fatty liver disease.
  • The discussion includes an analysis of various genome delivery methods, highlighting their advantages and limitations for effective gene editing.

Key Points:

  • Gene variants significantly influence the development and progression of both NAFLD and ALD.
  • CRISPR/Cas9 and related technologies offer powerful tools for modeling the genetic underpinnings of fatty liver diseases.
  • Selecting appropriate genome editing tools and delivery methods is crucial for developing accurate disease models.

Conclusions:

  • Advanced genome editing strategies are pivotal for creating precise models of NAFLD and ALD.
  • These models will accelerate the understanding of disease mechanisms and the discovery of targeted therapeutics.
  • This review provides guidance for selecting optimal genome editing approaches to advance fatty liver disease treatment development.