Calcineurin/NFAT Coupling Participates in Pathological, but not Physiological, Cardiac Hypertrophy

By B. Wilkins, Yan Dai, O. Bueno, Stephanie A. Parsons, Jian Xu, D. Plank, F. Jones, T. Kimball, J. Molkentin. Circulation Research, 2004

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Disruption of coordinated cardiac hypertrophy and angiogenesis contributes to the transition to heart failure. (2005, neutral): “In the heart, Akt is an important positive regulator of normal postnatal cardiac growth (19) and is also activated by exercise training (20–22), by pressure overload (23), and in diseased human hearts (24).”
Cardiovascular Effects and Benefits of Exercise (2018, background): “Other transcriptional pathways known to be activated by pathologic stimuli and cardiac hypertrophy, such as NFATc2, are decreased in exercise models (79, 84), suggesting that some signaling pathways activated during exercise-induced growth program may directly antagonize specific factors that promot”
Regulation of cardiac hypertrophy by intracellular signalling pathways (2006, background): “Although one study failed to observe NFAT activation in response to swimming exercise in mice (a stimulus for physiological heart growth”
Cell and Molecular Biology (2009, positive): “It could be demonstrated by the use of a NFAT-luciferase reporter construct, that NFAT is not upregulated during physiological hypertrophy, induced by exercise or stimulation with insulin-like growth factor-1 (IGF-1) (Wilkins et al., 2004).”
Chronic inhibition of cyclic GMP phosphodiesterase 5A prevents and reverses cardiac hypertrophy (2005, background): “, yet is not associated with calcineurin costimulatio”