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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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| Asıl Yazarlar: | , , , , , |
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| Materyal Türü: | Artigo |
| Dil: | Inglês |
| Baskı/Yayın Bilgisi: |
2014
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| Konular: | |
| Online Erişim: | 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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