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Deficiency of cardiac Acyl-CoA synthetase-1 induces diastolic dysfunction, but pathologic hypertrophy is reversed by rapamycin

In mice with temporally-induced cardiac-specific deficiency of acyl-CoA synthetase-1 (Acsl1(H−/−)), the heart is unable to oxidize long-chain fatty acids and relies primarily on glucose for energy. These metabolic changes result in the development of both a spontaneous cardiac hypertrophy and increa...

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Wedi'i Gadw mewn:
Manylion Llyfryddiaeth
Prif Awduron: Paul, David S., Grevengoed, Trisha J., Pascual, Florencia, Ellis, Jessica M., Willis, Monte S., Coleman, Rosalind A.
Fformat: Artigo
Iaith:Inglês
Cyhoeddwyd: 2014
Pynciau:
Mynediad Ar-lein:https://ncbi.nlm.nih.gov/pmc/articles/PMC4047709/
https://ncbi.nlm.nih.gov/pubmed/24631848
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.bbalip.2014.03.001
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