Why the study?
It was not clear whether apolipoprotein E has a role in the development of non-ischemic cardiomyopathy.
Does apolipoprotein E deficiency induce non-ischemic cardiomyopathy during aging in mice?
Does apolipoprotein E deficiency induce non-ischemic cardiomyopathy during aging in mice?
ApoE deficiency in mice induces mild changes in left ventricular cardiac function during aging, leading to diastolic dysfunction and potentially heart failure with preserved ejection fraction, even without a high-fat diet.
No cardiomyopathy in aged apoE-deficient mice; leaves open apoE's role in human non-ischemic cardiomyopathy.
BACKGROUND: Apolipoprotein (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 RESULTS: Serial 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. CONCLUSION: Even 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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Liehn et al. (2021) studied this question.
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