GRK2 compromises cardiomyocyte mitochondrial function by diminishing fatty acid-mediated oxygen consumption and increasing superoxide levels
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- 作者：Priscila Y. Sato ; J. Kurt Chuprun ; Jessica Ibetti ; Alessandro Cannavo ; Konstantinos Drosatos ; John W. Elrod ; Walter J. Koch ; Walter.Koch@temple.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：GRK2 ; Cardiomyocytes ; Mitochondria ; Respiration
- 刊名：Journal of Molecular and Cellular Cardiology
- 出版年：2015
- 出版时间：December 2015
- 年：2015
- 卷：89
- 期：part_PB
- 页码：360-364
- 全文大小：771 K
文摘
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Mitochondrial GRK2 is localized to multiple sub-mitochondrial locations.
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Overexpression of GRK2 in cardiomyocytes increases superoxide levels and impairs fatty acid-driven oxygen consumption rate.
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GRK2 kinase activity is necessary for the deleterious effect on mitochondrial energy dynamics.
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βARKct, a peptide inhibitor of GRK2, enhances basal oxygen consumption rates and ATP production.