Key result
The transcription factor FoxO1 is a critical mediator of exercise-induced physiological cardiac hypertrophy, with potential implications for treating heart failure.
Why the study?
Regulators of exercise-induced physiological cardiac hypertrophy are promising heart failure targets, but the transcriptional regulation of physiological hypertrophy has remained largely elusive.
Answers are grounded in this paper and cite their sources.
Positions FoxO1 as candidate target for exercise-mimetic HF therapies; leaves open validation in human cardiac remodeling.
Regulators of exercise-induced physiological cardiac hypertrophy and protection are considered promising targets for the treatment of heart failure. Unlike pathological hypertrophy, the transcriptional regulation of physiological hypertrophy has remained largely elusive. To our knowledge, this is the first study to show that the transcription factor FoxO1 is a critical mediator of exercise-induced cardiac hypertrophy. Given that exercise-induced hypertrophy is protective, this finding has important implications when one is considering FoxO1 as a target for treating the diseased heart.
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Weeks et al. (2021) studied Cardiac hypertrophy. FoxO1 was evaluated on Exercise-induced cardiac hypertrophy. The transcription factor FoxO1 is a critical mediator of exercise-induced physiological cardiac hypertrophy, with potential implications for treating heart failure.
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