Key result
Swimming-induced hypertrophy preserves cardiac function without GRK5 nuclear accumulation in post-TAC mice.
Why the study?
The role of GRK5 in physiological cardiac hypertrophy and its nuclear activity compared to pathological hypertrophy was unclear.
Does GRK5 nuclear accumulation occur during physiological swimming-induced hypertrophy in mice?
Does GRK5 nuclear accumulation occur during physiological swimming-induced hypertrophy in mice?
Noncanonical nuclear activity of GRK5 is a pathological mediator after stress but is not induced during physiological hypertrophy.
GRK5 nuclear accumulation is absent during physiological hypertrophy in GRK5-overexpressing mice; leaves open selective nuclear GRK5 targeting in human pathological remodeling.
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Traynham et al. (2015) studied Cardiac hypertrophy. 21-day high-intensity swim protocol vs. No swim sham controls or transverse aortic constriction (TAC) was evaluated on Cardiac growth and nuclear localization of GRK5. Physiological swimming-induced hypertrophy did not induce GRK5 nuclear accumulation and preserved cardiac function in post-TAC transgenic GRK5 mice.
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