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

ABSTRACT Because hearts with a temporally induced knockout of acyl‐CoA synthetase 1 (Acsl1T‐/‐) 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 incre...

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