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Updated: Jun 20, 2026

A Familial Hypercholesterolemia Human Liver Chimeric Mouse Model Using Induced Pluripotent Stem Cell-derived Hepatocytes

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Retinal findings in familial hypercholesterolemia: An exploratory case-control study.

Gisle Langslet¹, Synne Kollstad², Øystein Kalsnes Jørstad^3,4

¹Lipid Clinic, Oslo University Hospital, Oslo, Norway.

Atherosclerosis Plus

|June 19, 2026

Summary

Patients with familial hypercholesterolemia (FH) do not show increased retinal arteriolosclerosis. This study found no link between FH, high LDL-C, and damage to small arteries in the retina.

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Area of Science:

Ophthalmology
Cardiology
Genetics

Background:

Familial hypercholesterolemia (FH) causes high LDL-C from birth, increasing cardiovascular risk via atherosclerosis.
The impact of elevated LDL-C on smaller arteries, like retinal arterioles, is less understood.
Retinal arterioles may stiffen and thicken due to high LDL-C.

Purpose of the Study:

To investigate retinal arteriolosclerosis in FH patients versus controls.
To explore associations between retinal arteriolosclerosis and lipid levels, demographics, and treatment duration.

Main Methods:

Compared 50 FH patients (40-70 yrs, normotensive, non-smokers) with 30 controls.
Excluded participants with diabetes or vascular retinal disease.
Assessed retinal arteriolosclerosis using Scheie classification on fundus photographs.

Main Results:

No significant difference in retinal arteriolosclerosis prevalence between FH patients and controls.
Current lipid levels, age, sex, statin use, or duration of lipid-lowering treatment did not correlate with retinal arteriolosclerosis.

Conclusions:

FH patients do not exhibit a higher prevalence of retinal arteriolosclerosis compared to individuals without FH.
Elevated LDL-C in FH may not significantly impact retinal arteriolosclerosis in this cohort.