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Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase01:11

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Genetic polymorphisms in drug targets have emerged as critical determinants of interindividual variability in drug response and toxicity. Pharmacogenomic investigations increasingly focus on identifying these variations to personalize and optimize therapeutic interventions. A drug target may be a receptor, enzyme, or signaling protein involved in pharmacologic responses or disease-related pathways. While early pharmacogenetic studies focused primarily on drug metabolism, current research...

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Aortic Single-Cell Transcriptome Analysis Reveals ApoE-Isoform-Specific Influences on Vascular Disease.

David Y Hui1, Jeyashree Alagarsamy1, April Haller1

  • 1Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, Cincinnati, OH 45237, USA.

International Journal of Molecular Sciences
|June 26, 2026
PubMed
Summary

Apolipoprotein E2 (apoE2) accelerates atherosclerosis via hyperlipidemia and inflammation, while apoE4 enhances vascular inflammation without causing hyperlipidemia. Understanding these distinct mechanisms is crucial for developing targeted atherosclerosis therapies.

Keywords:
apolipoprotein Eatherosclerosisinflammationintracellular lipid accumulationsingle-cell transcriptome

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Isolation and Profiling of Human Primary Mesenteric Arterial Endothelial Cells at the Transcriptome Level
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Isolation and Profiling of Human Primary Mesenteric Arterial Endothelial Cells at the Transcriptome Level
09:45

Isolation and Profiling of Human Primary Mesenteric Arterial Endothelial Cells at the Transcriptome Level

Published on: March 14, 2022

Area of Science:

  • Cardiovascular Biology
  • Genetics
  • Immunology

Background:

  • The human apolipoprotein E (APOE) gene has three major alleles: APOE2, APOE3, and APOE4.
  • Both apoE2 and apoE4 are linked to increased risk of atherosclerosis.
  • The precise mechanisms by which apoE2 and apoE4 influence atherosclerosis remain incompletely understood.

Purpose of the Study:

  • To investigate the distinct molecular mechanisms by which apoE2 and apoE4 contribute to atherosclerosis development.
  • To compare the effects of apoE2, apoE3, and apoE4 on vascular health and inflammation in response to a high-fat diet.

Main Methods:

  • Utilized human APOE2, APOE3, and APOE4 gene replacement mouse models.
  • Administered a Western-type high-fat, high-cholesterol diet for 16 weeks.
  • Employed single-cell RNA sequencing (scRNA-seq) to analyze aortic cell populations.

Main Results:

  • APOE2 mice developed hyperlipidemia and significant atherosclerosis, unlike APOE3 and APOE4 mice.
  • Both APOE2 and APOE4 mice exhibited increased vascular inflammation.
  • scRNA-seq revealed APOE2-associated cells were enriched in lipid accumulation and inflammation genes.
  • APOE4-associated cells showed elevated oxidative stress, endoplasmic reticulum stress, and inflammatory responses.

Conclusions:

  • ApoE2 promotes atherosclerosis by driving diet-induced hyperlipidemia and inflammation.
  • ApoE4 contributes to atherosclerosis by enhancing vascular inflammation, potentially priming the vasculature.
  • Distinct mechanisms of apoE2 and apoE4 highlight the importance of apoE genotype in atherosclerosis therapeutics.