AMPK in cardiac fibrosis and repair: Actions beyond metabolic regulation
(2016) Journal of Molecular and Cellular Cardiology — Vol. 91, p. 188-200 (2016)
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- Abstract
- Cardiac muscle is characterized by its metabolic flexibility, which means that it uses various substrates for energy production, regulating their utilization in terms of their availability and hormonal status. This metabolic flexibility is essential to maintain cardiac function. Reduction of this metabolic flexibility participates in the development of cardiac diseases. Insulin resistance and more generally diabetes are clearly linked to the development of a cardiac dysfunction called diabetic cardiomyopathy that can induce heart failure, independently of coronary artery disease and hypertension. The reestablishment of regular glucose uptake and utilization by restoring insulin sensitivity has been proposed to improve cardiac function of the diabetic heart. Insulin sensitivity can be improved by blocking the source of insulin resistance or by modulating insulin signaling and signaling pathways involved in the development of insulin resistance. A recognized cellular fuel gauge called AMP-activated protein kinase could play an important role in such therapies.
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Daskalopoulos, E.-P., Dufeys, C., Bertrand, L., Beauloye, C., & Horman, S. (2016). AMPK in cardiac fibrosis and repair: Actions beyond metabolic regulation. Journal of Molecular and Cellular Cardiology, 91, 188-200. https://doi.org/10.1016/j.yjmcc.2016.01.001 (Original work published 2016)