1. Altered expression levels of autophagy-associated proteins during exercise preconditioning indicate the involvement of autophagy in cardioprotection against exercise-induced myocardial injury
- Author
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Yuan, Jian-Qi, Yuan, Yang, Pan, Shan-Shan, and Cai, Ke
- Subjects
Exercise ,Immunohistochemistry ,Ischemia ,Cathepsins ,Proteins ,Heart ,Psychology and mental health - Abstract
Exercise has been reported to induce autophagy. We hypothesized that exercise preconditioning (EP)-related autophagy in cardiomyocytes could be attributed to intermittent ischemia-hypoxia, allowing the heart to be protected for subsequent high-intensity exercise (HE). We applied approaches, chromotrope-2R brilliant green (C-2R BG) staining and plasma cTnI levels measuring, to characterize two periods of cardioprotection after EP: early EP (EEP) and late EP (LEP). Further addressing the relationship between ischemia-hypoxia and autophagy, key proteins, Beclin1, LC3, Cathepsin D, and p62, were determined by immunohistochemical staining, western blotting, and by their adjacent slices with C-2R BG. Results indicated that exercise-induced ischemia-hypoxia is a key factor in Beclin1-dependent autophagy. High-intensity exercise was associated with the impairment of autophagy due to high levels of LC3II and unchanged levels of p62, intermittent ischemia-hypoxia by EP itself plays a key role in autophagy, which resulted in more favorable cellular effects during EEP-cardioprotection compared to LEP. Keywords: Exercise preconditioning, Ischemia-hypoxia, Autophagy, Cardioprotection, Author(s): Jian-Qi Yuan[sup.1], Yang Yuan[sup.1], Shan-Shan Pan[sup.1] and Ke Cai[sup.1] Background Strategies that encourage endogenous cardiac adaptations have increasingly been used as non-pharmacological therapies to mitigate the risks of cardiovascular [...]
- Published
- 2020
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