Abstract
Cancer cachexia is a syndrome experienced by many patients with cancer. Exercise can act as an autophagy modulator, and thus holds the potential to be used to treat cancer cachexia. Autophagy imbalance plays an important role in cancer cachexia, and is correlated to skeletal and cardiac muscle atrophy and energy-wasting in the liver. The molecular mechanism of autophagy modulation in different types of exercise has not yet been clearly defined. This review aims to elaborate on the role of exercise in modulating autophagy in cancer cachexia. We evaluated nine studies in the literature and found a potential correlation between the type of exercise and autophagy modulation. Combined exercise or aerobic exercise alone seems more beneficial than resistance exercise alone in cancer cachexia. Looking ahead, determining the physiological role of autophagy modulated by exercise will support the development of a new medical approach for treating cancer cachexia. In addition, the harmonization of the exercise type, intensity, and duration might play a key role in optimizing the autophagy levels to preserve muscle function and regulate energy utilization in the liver.
Highlights
Introduction iationsPatients with cancer usually experience cachexia; cancer cachexia is a multifactorial syndrome correlated with cancer, characterized by skeletal muscle decline that cannot be fully recovered by nutritional support, and eventually leads to dysfunction of the muscle [1,2]
After 45 days of moderate treadmill exercise, there was a reduction in the mRNA levels of BNIP3, which supported the hypothesis that aerobic exercise training might be beneficial in reducing the cardiac remodeling of cancer cachexia by modulating autophagy [19]
Careful evaluation and personalization before choosing the type, intensity, and duration of exercise to cope with cancer cachexia might leverage the benefits of exercise
Summary
Autophagy is a physiological intracellular process that consists of the destruction and elimination of substances, such as misfolded proteins or organelles, to adapt or maintain cellular homeostasis. Beclin-1, a key upstream regulator of and Beclin-1 in the skeletal muscle of C26 tumor-bearing mice These findings were folautophagic sequestration, was significantly higher, implying that autophagy activation is a lowed by increased p62 and unchanged p62 muscle levels,p62 suggesting a in reduction key protein to the early event in tumor-induced depletion; accumulated a similar manner to Beclin-1. Beclin-1, a key upstream regulator of autophagic sequestration, was significantly higher, implying that autophagy activation is a key to the early event in tumor-induced muscle depletion; p62 accumulated in a similar
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