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Loss of long-chain acyl-CoA synthetase isoform 1 impairs cardiac autophagy and mitochondrial structure through mechanistic target of rapamycin complex 1 activation

Because hearts with a temporally induced knockout of acyl-CoA synthetase 1 (Acsl1(T−/−)) are virtually unable to oxidize fatty acids, glucose use increases 8-fold to compensate. This metabolic switch activates mechanistic target of rapamycin complex 1 (mTORC1), which initiates growth by increasing p...

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Dettagli Bibliografici
Pubblicato in:FASEB J
Autori principali: Grevengoed, Trisha J., Cooper, Daniel E., Young, Pamela A., Ellis, Jessica M., Coleman, Rosalind A.
Natura: Artigo
Lingua:Inglês
Pubblicazione: Federation of American Societies for Experimental Biology 2015
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Accesso online:https://ncbi.nlm.nih.gov/pmc/articles/PMC4608904/
https://ncbi.nlm.nih.gov/pubmed/26220174
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1096/fj.15-272732
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