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P66shc and its role in ischemic cardiovascular diseases

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Abstract

Oxidative stress caused by an imbalance in the formation and removal of reactive oxygen species (ROS) plays an important role in the development of several cardiovascular diseases. ROS originate from various cellular origins; however, the highest amount of ROS is produced by mitochondria. One of the proteins contributing to mitochondrial ROS formation is the adaptor protein p66shc, which upon cellular stresses translocates from the cytosol to the mitochondria. In the present review, we focus on the role of p66shc in longevity, in the development of cardiovascular diseases including diabetes, atherosclerosis and its risk factors, myocardial ischemia/reperfusion injury and the protection from it by ischemic preconditioning. Also, the contribution of p66shc towards cerebral pathologies and the potential of the protein as a therapeutic target for the treatment of the aforementioned diseases are discussed.

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Acknowledgements

RS was funded by the German Research Foundation: Project number 268555672-SFB-B05 and the Cardio-Pulmonary Institute (CPI), EXC 2026, Project ID: 390649896.

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Correspondence to Rainer Schulz.

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Rainer Schulz received honoraries for lectures provided to AstraZeneca, Recordati and Sanofi.

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All applicable international, national, and/or institutional guidelines for the care and use of animals were followed. The study was approved by local authorities (“Regierungspräsidium Giessen” (G91-2017) and the animal welfare office of the Justus-Liebig-University Giessen). This article does not contain any studies with human participants performed by any of the authors.

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Boengler, K., Bornbaum, J., Schlüter, KD. et al. P66shc and its role in ischemic cardiovascular diseases. Basic Res Cardiol 114, 29 (2019). https://doi.org/10.1007/s00395-019-0738-x

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