Litcius/Paper detail

FoxO1 is required for physiological cardiac hypertrophy induced by exercise but not by constitutively active PI3K

Kate L. Weeks, Yow Keat Tham, Suzan Yıldız, Yonali Alexander, D. Donner, Helen Kiriazis, Claudia A. Harmawan, Amy T. Hsu, Bianca C. Bernardo, Aya Matsumoto, Ronald A. DePinho, E. Dale Abel, Elizabeth A. Woodcock, Julie R. McMullen

2021American Journal of Physiology-Heart and Circulatory Physiology35 citationsDOIOpen Access PDF

Abstract

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.

Topics & Concepts

FOXO1Muscle hypertrophyCardiac hypertrophyHeart failurePathologicalMediatorTranscription factorMedicineInternal medicineEndocrinologyCardiologyBiologyGeneBiochemistryFOXO transcription factor regulationAdipose Tissue and MetabolismCardiovascular Effects of Exercise