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September 1, 1994Arteriosclerosis and Thrombosis A Journal of Vascular Biology

Pathology of atheromatous lesions in inbred and genetically engineered mice. Genetic determination of arterial calcification.

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Population

Various inbred mouse strains fed a high-fat, high-cholesterol diet and two genetically engineered strains on…

Comparison

High-fat, high-cholesterol diet or genetic… vs Normal arteries / different mouse strains

Design

Preclinical

Authors

JQJ. H. QiaoThe Fourth People's Hospital of Zibo CityPXPeizhen XieGuangxi Medical UniversityMFMichael C. FishbeinElectrophysiology

Discussion

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Implication

Site-specific genetic effects on atherosclerosis and calcification in mice; leaves open translation to human coronary disease patterns.

Structured PICO

P
Population
Various inbred mouse strains fed a high-fat, high-cholesterol diet and two genetically engineered strains (apolipoprotein E null mutation, apolipoprotein A-II transgenic) on a low-fat chow diet
I
Intervention
High-fat, high-cholesterol diet or genetic engineering (ApoE null, ApoA-II transgenic)
C
Comparator
Normal arteries / different mouse strains
O
Outcome
Pathology of atheromatous lesions (anatomic locations, lesion severity, calcification, lipofuscin deposition, cellular and molecular compositions)surrogate

This preclinical study demonstrates that genetic factors influence the development and calcification of atheromatous lesions, with distinct genetic determinants for coronary versus aortic lesions.

Cite This Study

Qiao et al. (1994) studied this question.

synapsesocial.com/papers/6a6f227c2163a0a01bc3785fhttps://doi.org/10.1161/01.atv.14.9.1480

Topics

Coronary artery diseaseCoronary CT angiography
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