Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Diabetic atherosclerosis mouse models.

Kenneth K Wu1, Youming Huan

  • 1Department of Cardiovascular Disease, Merck Research Laboratories, RY 80W-250, 126 East Lincoln Avenue, Rahway, NJ 07065, USA. ken_wu@merck.com

Atherosclerosis
|September 19, 2006
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Smooth muscle-specific expression of hydroxyindole O-methyltransferase reduces arterial injury-induced intimal hyperplasia.

Journal of biomedical science·2025
Same author

5-Methoxytryptophan attenuates oxidative stress-induced downregulation of PINK1 and mitigates mitochondrial damage and apoptosis in cardiac myocytes.

Free radical biology & medicine·2025
Same author

5-Methoxytryptophan Protects against Toll-Like Receptor 2-Mediated Renal Tissue Inflammation and Fibrosis in a Murine Unilateral Ureteral Obstruction Model.

Journal of innate immunity·2025
Same author

Extracellular Succinate: A Physiological Messenger and a Pathological Trigger.

International journal of molecular sciences·2023
Same author

Cancer-derived extracellular succinate: a driver of cancer metastasis.

Journal of biomedical science·2022
Same author

Control of Tissue Fibrosis by 5-Methoxytryptophan, an Innate Anti-Inflammatory Metabolite.

Frontiers in pharmacology·2021
Same journal

Optimized flow cytometry assay for functional characterization of variants of uncertain significance in familial hypercholesterolemia.

Atherosclerosis·2026
Same journal

Causal insights of modifiable cardiovascular risk factors for dementia risk - potential for efficient prevention and improved brain health.

Atherosclerosis·2026
Same journal

Serial OCT-based coronary physiology and plaque composition in vessels with nonobstructive coronary lesions following intensive lipid-lowering therapy: YELLOW III sub-study.

Atherosclerosis·2026
Same journal

Earliest age to detect lifetime cardiometabolic health stratification in children.

Atherosclerosis·2026
Same journal

Sympathetic neurons exacerbate atherosclerosis by modulating macrophage function via the NPY/Y1R axis.

Atherosclerosis·2026
Same journal

Optimizing lipoprotein(a) testing for immediate clinical impact in primary prevention.

Atherosclerosis·2026
See all related articles

Diabetic atherosclerosis mouse models are crucial for research, but no single model perfectly replicates human disease. This review evaluates existing models to guide selection for studying diabetes-accelerated atherosclerosis and testing therapies.

Area of Science:

  • Cardiovascular Research
  • Metabolic Disease Research
  • Animal Models in Atherosclerosis

Background:

  • Coronary heart disease (CHD) from atherosclerosis is a leading cause of death, particularly accelerated in diabetic patients.
  • Understanding diabetes-accelerated atherosclerosis is critical for developing effective treatments.
  • Mice are the primary animal model for studying diabetic atherosclerosis due to their advantages.

Purpose of the Study:

  • To review and characterize common diabetic atherosclerosis mouse models.
  • To assess how well these models mimic human diabetic atherosclerosis.
  • To guide the selection of appropriate models for research and therapeutic evaluation.

Main Methods:

  • Review of existing literature on diabetic atherosclerosis mouse models.

Related Experiment Videos

  • Analysis of models based on retention of diabetic condition.
  • Evaluation of models regarding acceleration of atherosclerosis and atherogenic inflammation.
  • Assessment of model response to medical interventions.

    • Main Results:

    • Several diabetic atherosclerosis mouse models have been developed.
    • No single model perfectly recapitulates human diabetic atherosclerosis.
    • Models vary in their ability to maintain diabetes, accelerate atherosclerosis, and respond to treatments.

    Conclusions:

    • Careful selection of diabetic atherosclerosis mouse models is essential for accurate research.
    • Understanding model-specific characteristics aids in studying disease mechanisms and evaluating therapies.
    • Further refinement of models is needed to better approximate human diabetic atherosclerosis.