Key result
Exercise preconditioning attenuated TAC-induced cardiac hypertrophy, fibrosis, and systolic dysfunction in mice, an effect that was completely abolished in Nrf2 knockout mice.
Why the study?
Exercise protects against pathological cardiac hypertrophy and heart failure, yet the underlying mechanisms remain unclear.
Does exercise preconditioning attenuate TAC-induced cardiac hypertrophy and myocardial injury through activating NRF2 in mice?
Population
Wild-type and Nrf2-KO mice subjected to transverse aortic constriction
Comparison
Exercise preconditioning vs sedentary control
Design
Preclinical animal study
Authors
Loading...
Supports Nrf2 mediation of exercise preconditioning in murine TAC; hypothesis-generating for human HF translation studies.
Does exercise preconditioning attenuate TAC-induced cardiac hypertrophy and myocardial injury through activating NRF2 in mice?
Exercise preconditioning protects against pressure overload-induced cardiac hypertrophy and dysfunction primarily through Nrf2 activation and suppression of oxidative stress.
Ni et al. (2025) studied TAC-induced cardiac hypertrophy and heart failure. Exercise-preconditioning vs. Sedentary control was evaluated on Cardiac hypertrophy, fibrosis, systolic dysfunction, and oxidative stress. Exercise preconditioning attenuated TAC-induced cardiac hypertrophy, fibrosis, and systolic dysfunction in mice, an effect that was completely abolished in Nrf2 knockout mice.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: