| First Author | Ma X | Year | 2015 |
| Journal | PLoS One | Volume | 10 |
| Issue | 6 | Pages | e0129971 |
| PubMed ID | 26068068 | Mgi Jnum | J:237694 |
| Mgi Id | MGI:5816641 | Doi | 10.1371/journal.pone.0129971 |
| Citation | Ma X, et al. (2015) Cardiac Fibrosis Alleviated by Exercise Training Is AMPK-Dependent. PLoS One 10(6):e0129971 |
| abstractText | Regular exercise can protect the heart against external stimuli, but the mechanism is not well understood. We determined the role of adenosine monophosphate-activated protein kinase (AMPK) in regulating swimming exercise-mediated cardiac protection against beta-adrenergic receptor overstimulation with isoproterenol (ISO) in mice. Ten-week-old AMPKalpha2+/+ and AMPKalpha2-knockout (AMPKalpha2-/-) littermates were subjected to 4 weeks of swimming training (50 min daily, 6 days a week) or housed under sedentary conditions. The mice received daily subcutaneous injection of ISO (5 mg/kg/d), a nonselective beta-adrenergic receptor agonist, during the last 2 weeks of swimming training. Swimming training alleviated ISO-induced cardiac fibrosis in AMPKalpha2+/+ mice but not AMPKalpha2-/- mice. Swimming training activated cardiac AMPK in AMPKalpha2+/+ mice. Furthermore, swimming training attenuated ISO-induced production of reactive oxygen species (ROS) and expression of NADPH oxidase and promoted the expression of antioxidant enzymes in AMPKalpha2+/+ mice but not AMPKalpha2-/- mice. In conclusion, swimming training attenuates ISO-induced cardiac fibrosis by inhibiting the NADPH oxidase-ROS pathway mediated by AMPK activation. Our findings provide a new mechanism for the cardioprotective effects of exercise. |
