Paper of the Month-(June 2018) from Dr. Hood's research group

Chen CCW, Erlich AT, Crilly MJ, Hood DA. Parkin is required for exercise-induced mitophagy in muscle: impact of aging. Am J Physiol Endocrinol Metab. 2018 May 29. doi: 10.1152/ajpendo.00391.2017. [Epub ahead of print]


Significance of the research:

Physical inactivity is an increasing contributing factor to several metabolic disorders including type II diabetes, obesity and cardiovascular disease. Regular exercise is a common prescription to combat against these disorders. However, the molecular mechanisms that underly the beneficial effects of exercise remain poorly understood. Mitochondria are energy-producing components in skeletal muscle cells that are highly active in producing energy during exercise. However, when mitochondria are unable to generate energy efficiently, they are swiftly removed from the cell in a breakdown process known as mitophagy. In this study, we have identified Parkin, a protein mutated in Parkinson’s disease, as an important factor required for mitophagy in muscle during exercise. We found that the absence of Parkin reduced the ability of muscle to breakdown dysfunctional mitochondria during exercise.  Thus, our results describe an important function for Parkin in muscle, and provide a greater understanding of the cellular underpinnings of the positive effects of exercise on muscle health.

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