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Related Experiment Video

Updated: Feb 15, 2026

A Familial Hypercholesterolemia Human Liver Chimeric Mouse Model Using Induced Pluripotent Stem Cell-derived Hepatocytes
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Oxidative burden in familial hypercholesterolemia.

Hamid Mollazadeh1,2, Federico Carbone3, Fabrizio Montecucco3,4,5

  • 1Department of Physiology and Pharmacology, School of Medicine, North Khorasan University of Medical Sciences, Bojnurd, Iran.

Journal of Cellular Physiology
|January 12, 2018
PubMed
Summary
This summary is machine-generated.

Familial hypercholesterolemia (FH) causes high LDL cholesterol, accelerating atherosclerosis. Targeting oxidative stress (OS) may reduce this cardiovascular risk in FH patients.

Keywords:
LDLatherosclerosisdyslipidemiafamilial hypercholesterolemiaoxidative stress

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Area of Science:

  • Cardiovascular Science
  • Genetics
  • Biochemistry

Background:

  • Familial hypercholesterolemia (FH) is a genetic disorder causing high LDL cholesterol (LDL-c).
  • FH accelerates atherosclerosis and is a leading hereditary cause of premature coronary heart disease.
  • Mutations in the LDL receptor gene are the hallmark of FH, leading to elevated circulating LDLs.

Purpose of the Study:

  • To review the pathophysiological mechanisms linking FH to reactive oxygen species (ROS) generation.
  • To update knowledge on the detrimental impact of ROS on atherosclerotic pathophysiology in FH.
  • To examine the role of oxidative stress (OS) in FH-related inflammation and atherosclerosis.

Main Methods:

  • Narrative review of experimental and clinical data.
  • Analysis of the association between FH and OS.
  • Evaluation of OS as a promoter of inflammation and atherosclerosis.

Main Results:

  • FH promotes ROS generation, a key factor in atherosclerosis development.
  • Oxidized LDL, malondialdehyde, ROS, and isoprostanes are key mediators of oxidative injury in FH.
  • Oxidative stress plays a significant role in FH-related inflammation and atherogenesis.

Conclusions:

  • Targeting oxidative stress presents a promising therapeutic strategy for reducing atherogenesis in FH patients.
  • Understanding the link between FH, ROS, and atherosclerosis is crucial for developing new treatments.