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Related Experiment Video

Updated: May 23, 2026

Quantification of Atherosclerosis in Mice

Quantification of Atherosclerosis in Mice

Published on: June 12, 2019

Genetics of atherosclerosis.

Aldons J Lusis¹

¹University of California, Los Angeles, Department of Medicine/Division of Cardiology, Los Angeles, CA 90095-1679, USA. jlusis@mednet.ucla.edu

Trends in Genetics : TIG

|April 7, 2012

Summary

Genome-wide association studies (GWAS) reveal new genes linked to cardiovascular disease, expanding our understanding beyond known pathways like lipoproteins. Further research is needed to fully understand atherosclerosis mechanisms.

Area of Science:

Genetics and Molecular Biology
Cardiovascular Research
Genomics

Background:

Genome-wide association studies (GWAS) have identified numerous genes associated with common cardiovascular disease (CVD) traits.
Previous knowledge emphasized the role of lipoproteins, but GWAS revealed many novel genes not linked to known atherosclerosis pathways.
Understanding the genetic underpinnings of CVD remains incomplete.

Purpose of the Study:

To review the impact of GWAS on understanding cardiovascular disease genetics.
To summarize pre-GWAS knowledge and highlight discoveries made through GWAS.
To discuss limitations of current GWAS approaches and propose future strategies for mechanistic insights into atherosclerosis.

Main Methods:

Review of human and animal model studies.

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A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

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Quantification of Atherosclerosis in Mice

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Published on: June 12, 2019

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology

Published on: May 6, 2014

Analysis of findings from genome-wide association studies (GWAS).

Synthesis of existing literature on cardiovascular disease genetics and atherosclerosis.

Main Results:

GWAS confirmed the importance of established factors like lipoproteins in CVD.
A significant number of newly identified genes associated with CVD were not previously linked to atherosclerosis.
GWAS have substantially altered the landscape of cardiovascular disease genetics research.

Conclusions:

GWAS have provided unbiased evidence for novel genetic contributors to cardiovascular disease.
There is a critical need for further research to elucidate the mechanisms of atherosclerosis involving newly discovered genes.
Future strategies should aim to integrate GWAS findings with functional studies for a comprehensive understanding of CVD.