ArticleDiscoveries (Craiova, Romania)
Heart function assessment during aging in apolipoprotein E knock-out mice.
Article in Discoveries (Craiova, Romania). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Apolipoprotein E ε3/ε4 and coronary artery disease: lipid and non-lipid mechanisms in personalized prevention - narrative review.Frontiers in cardiovascular medicine · 2026Review
- Assessing the cardioprotective effects of exercise in APOE mouse models using deep learning and photon-counting micro-CT.PloS one · 2025Article
- The causal effect of Alzheimer's disease and family history of Alzheimer's disease on non-ischemic cardiomyopathy and left ventricular structure and function: a Mendelian randomization study.Frontiers in genetics · 2024Article
- Human ApoE2 Endows Stronger Contractility in Rat Cardiomyocytes Enhancing Heart Function.Cells · 2023Article
- Advanced photon counting CT imaging pipeline for cardiac phenotyping of apolipoprotein E mouse models.PloS one · 2023Article
- Endogenous Modulation of Extracellular Matrix Collagen during Scar Formation after Myocardial Infarction.International journal of molecular sciences · 2022Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundApolipoprotein (apo) E isoforms have strong correlations with metabolic and cardiovascular diseases. However, it is not clear if apoE has a role in development of non-ischemic cardiomyopathy. Our study aims to analyze the involvement of apoE in non-ischemic cardiomyopathy. METHODS AND
resultsSerial echo-cardiographic measurements were performed in old wildtype and apoE deficient (apoE-/-) mice. Morphological and functional cardiac parameters were in normal range in both groups at the age of 12 month. At the age of 18 months, both groups had shown ventricular dilation and increased heart rates. However, the apoE-/- mice presented signs of diastolic dysfunction by hypertrophic changes in left ventricle, due probably to arterial hypertension. The right ventricle was not affected by age or genotype.
conclusionEven in the absence of high fat diet, apoE deficiency in mice induces mild changes in the cardiac function of the left ventricle during aging, by developing diastolic dysfunction, which leads to heart failure with preserved ejection fraction. However, further studies are necessary to conclude over the role of apoE in cardiac physiology and its involvement in development of heart failure.
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