Cardioprotection and lifespan extension by the natural polyamine spermidine
Nature Medicine, 2016
Eisenberg T., Abdellatif M., Schroeder S., Primessnig U., Stekovic S., Pendl T., Harger A., Schipke J., Zimmermann A., Schmidt A., Tong M., Ruckenstuhl C., Dammbrueck C., Gross A., Herbst V., Magnes C., Trausinger G., Narath S., Meinitzer A., Hu Z., Kirsch A., Eller K., Carmona-Gutierrez D., Büttner S., Pietrocola F., Knittelfelder O., Schrepfer E., Rockenfeller P., Simonini C., Rahn A., Horsch M., Moreth K., Beckers J., Fuchs H., Gailus-Durner V., Neff F., Janik D., Rathkolb B., Rozman J., de Angelis M., Moustafa T., Haemmerle G., Mayr M., Willeit P., von Frieling-Salewsky M., Pieske B., Scorrano L., Pieber T., Pechlaner R., Willeit J., Sigrist S., Linke W., Mühlfeld C., Sadoshima J., Dengjel J., Kiechl S., Kroemer G., Sedej S., Madeo F.
| Disease area | Application area | Sample type | Products |
|---|---|---|---|
CVD | Pathophysiology | Serum |  Olink Target 96 |
Abstract
Fascinating study that suggests that simple dietary supplementation with spermidine may provide a strategy for protection against cardiovascular disease. Heart disease is strongly associated with aging, probably related to increasing cardiac hypertrophic remodeling. Studies suggest that autophagy may be able to minimize the functional decline of aging cardiomyocytes by degrading and recycling potentially toxic proteins as well as cytoplasmic components and dysfunctional organelles. Their earlier studies showed that the natural dietary polyamine, spermidine, extends lifespan and health span through induction of autophagy in yeast, flies and worms. In this study, they took this hypothesis into an experimental mouse & rat models to investigate the possible effects of spermidine on key biological processes and links to CVD. The vast majority of this paper focuses on the animal models, which showed that spermidine prolongs the life of the animals via improving cardial health parameters, and that this cardioprotective effect is dependent on autophagy. These dramatic effects in rodents were also assessed for human relevance by measuring clinical parameters in subjects where extensive dietary information was availabe, and where estimations of spermidine intake could therefore be estimated. This data showed a clear inverse correlation between spermidine intake and cardiac disease in humans. They then used the INF and CVD I panels to look at the relationship between spermidine intake and known CVD markers, again seeing an inverse relationship between dietary spermidne intake and protein expression. They infer that several such proteins showed this pattern, but only mention CHI3L1 and GFD-15 by name. [Note that while the Olink methodology is described in the Supplementary Materials, the only reference to the data is in one sentence in the Results section. No Olink data is shown, and the findings are not mentioned in the Discussion].