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SHR Neuro Krebs Kardio Lipid Stoffw Microb

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, AS; 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, MH; Moustafa, T; Haemmerle, G; Mayr, M; Willeit, P; von Frieling-Salewsky, M; Pieske, B; Scorrano, L; Pieber, T; Pechlaner, R; Willeit, J; Sigrist, SJ; Linke, WA; Mühlfeld, C; Sadoshima, J; Dengjel, J; Kiechl, S; Kroemer, G; Sedej, S; Madeo, F.
Cardioprotection and lifespan extension by the natural polyamine spermidine.
Nat Med. 2016; 22(12):1428-1438 Doi: 10.1038/nm.4222 [OPEN ACCESS]
Web of Science PubMed PUBMED Central FullText FullText_MUG


Führende Autor*innen der Med Uni Graz
Abdellatif Mahmoud
Sedej Simon
Co-Autor*innen der Med Uni Graz
Eller Kathrin
Harger Alexandra
Kirsch Alexander
Meinitzer Andreas
Moustafa Tarek
Pieber Thomas
Pieske Burkert Mathias
Primessnig Uwe
Rockenfeller Patrick
Schmidt Albrecht

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Aging is associated with an increased risk of cardiovascular disease and death. Here we show that oral supplementation of the natural polyamine spermidine extends the lifespan of mice and exerts cardioprotective effects, reducing cardiac hypertrophy and preserving diastolic function in old mice. Spermidine feeding enhanced cardiac autophagy, mitophagy and mitochondrial respiration, and it also improved the mechano-elastical properties of cardiomyocytes in vivo, coinciding with increased titin phosphorylation and suppressed subclinical inflammation. Spermidine feeding failed to provide cardioprotection in mice that lack the autophagy-related protein Atg5 in cardiomyocytes. In Dahl salt-sensitive rats that were fed a high-salt diet, a model for hypertension-induced congestive heart failure, spermidine feeding reduced systemic blood pressure, increased titin phosphorylation and prevented cardiac hypertrophy and a decline in diastolic function, thus delaying the progression to heart failure. In humans, high levels of dietary spermidine, as assessed from food questionnaires, correlated with reduced blood pressure and a lower incidence of cardiovascular disease. Our results suggest a new and feasible strategy for protection against cardiovascular disease.
Find related publications in this database (using NLM MeSH Indexing)
Adult -
Aged -
Aging - drug effects
Aging - immunology
Aging - metabolism
Animals -
Autophagy - drug effects
Autophagy-Related Protein 5 - genetics
Blood Pressure - drug effects
Cardiomegaly - diagnostic imaging
Cardiotonic Agents - pharmacology
Cardiovascular Diseases - epidemiology
Chromatography, High Pressure Liquid -
Connectin - drug effects
Connectin - metabolism
Cytokines - drug effects
Cytokines - immunology
Diastole -
Diet - statistics & numerical data
Echocardiography -
Female -
Gene Expression - drug effects
Glucose Tolerance Test -
Heart - diagnostic imaging
Heart - drug effects
Heart Failure -
Humans -
Immunoblotting -
Inflammation -
Longevity - drug effects
Male -
Mass Spectrometry -
Mice -
Middle Aged -
Mitochondria, Heart - drug effects
Mitochondria, Heart - metabolism
Mitochondrial Degradation - drug effects
Myocytes, Cardiac - drug effects
Phosphorylation - drug effects
Prospective Studies -
Rats -
Rats, Inbred Dahl -
Spermidine - pharmacology
Surveys and Questionnaires -

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