Key result
YAP regulates metabolic reprogramming in the heart during compensatory hypertrophy by upregulating GLUT1 and inducing glycolysis.
YAP acts as a regulator of metabolic reprogramming in the heart during compensatory hypertrophy by upregulating GLUT1, providing mechanistic insights that may help develop future therapies for heart failure.
Cardiomyocyte hypertrophy is an integral part of cardiac remodeling that occurs under physiological or pathological stresses. It can lead to heart failure in a pathological form or oppose functional deterioration in a compensatory one. The mechanisms underlying an adaptive outcome of hypertrophy are ill defined. In this issue of the JCI, Kashihara et al. explored the role of the Yes-associated protein 1 (YAP) transcription factor in the heart, using cell culturing and mouse models. YAP activity was found to be associated with changes in genes of the glycolytic and auxiliary pathways under stress. Notably, YAP upregulated glucose transporter 1 (GLUT1), and inhibition of GLUT1 blocked YAP-induced hypertrophy but worsened heart function. These findings suggest that YAP is a regulator of metabolic reprogramming in the heart during compensatory hypertrophy. This insight may help in the development of future therapies for heart failure.
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A 2022 study conducted an editorial in Cardiac hypertrophy and remodeling. YAP (Yes-associated protein 1) was evaluated. YAP regulates metabolic reprogramming in the heart during compensatory hypertrophy by upregulating GLUT1 and inducing glycolysis.
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