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♦ See referenced article, J. Biol. Chem. 2013, 288, 915–926
Loss-of-function mutations in the Parkin gene are known to lead to Parkinson disease. In neurons, Parkin is critical for removing dysfunctional mitochondria via autophagy. The protein is also expressed in the heart, but its role there is largely unknown. In this Paper of the Week, a team led by Åsa B. Gustafsson at the University of California, San Diego, used genetically engineered mice missing the Parkin gene. By comparing these mice with wild-type mice, they found that the absence of Parkin did not affect mitochondrial turnover under normal conditions. However, during stress conditions, such as a myocardial infarction that simulates a heart attack, the protein was necessary for the heart muscle, or myocardium, to adapt to the stress by helping to remove damaged mitochondria by autophagy. The data suggest that Parkin plays a critical role in repairing damage in cells after a heart attack.