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1. Dietary spermidine improves cognitive function

Author

Schroeder, Sabrina, Hofer, Sebastian, Zimmermann, Andreas, Pechlaner, Raimund, Dammbrueck, Christopher, Pendl, Tobias, Marcello, G. Mark, Pogatschnigg, Viktoria, Bergmann, Martina, Müller, Melanie, Gschiel, Verena, Ristic, Selena, Tadic, Jelena, Iwata, Keiko, Richter, Gesa, Farzi, Aitak, Üçal, Muammer, Schäfer, Ute, Poglitsch, Michael, Royer, Philipp, Mekis, Ronald, Agreiter, Marlene, Tölle, Regine, Sótonyi, Péter, Willeit, Johann, Mairhofer, Barbara, Niederkofler, Helga, Pallhuber, Irmgard, Rungger, Gregorio, Tilg, Herbert, Defrancesco, Michaela, Marksteiner, Josef, Sinner, Frank, Magnes, Christoph, Pieber, Thomas, Holzer, Peter, Kroemer, Guido, Carmona-Gutierrez, Didac, Scorrano, Luca, Dengjel, Jörn, Madl, Tobias, Sedej, Simon, Sigrist, Stephan, Rácz, Bence, Kiechl, Stefan, Eisenberg, Tobias, Madeo, Frank, Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université de Paris (UP), Institut Gustave Roussy (IGR), Hôpital Européen Georges Pompidou [APHP] (HEGP), and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)

Subjects
Male, autophagy, Spermidine, QH301-705.5, Ubiquitin-Protein Ligases, Autophagy-Related Protein 7, Oxidative Phosphorylation, memory, Mice, Cognition, Animals, Humans, Learning, Cognitive Dysfunction, dietary spermidine, Biology (General), cognitive function, Spatial Memory, Neurons, aging, mitochondria, mitophagy, Pink1, Brain, [SDV.NEU.SC]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Cognitive Sciences, Drosophila melanogaster, Gene Expression Regulation, Dietary Supplements, Female, Protein Kinases, [SDV.AEN]Life Sciences [q-bio]/Food and Nutrition, Signal Transduction
Abstract

International audience; Decreased cognitive performance is a hallmark of brain aging, but the underlying mechanisms and potential therapeutic avenues remain poorly understood. Recent studies have revealed health-protective and lifespan-extending effects of dietary spermidine, a natural autophagy-promoting polyamine. Here, we show that dietary spermidine passes the blood-brain barrier in mice and increases hippocampal eIF5A hypusination and mitochondrial function. Spermidine feeding in aged mice affects behavior in homecage environment tasks, improves spatial learning, and increases hippocampal respiratory competence. In a Drosophila aging model, spermidine boosts mitochondrial respiratory capacity, an effect that requires the autophagy regulator Atg7 and the mitophagy mediators Parkin and Pink1. Neuron-specific Pink1 knockdown abolishes spermidine-induced improvement of olfactory associative learning. This suggests that the maintenance of mitochondrial and autophagic function is essential for enhanced cognition by spermidine feeding. Finally, we show large-scale prospective data linking higher dietary spermidine intake with a reduced risk for cognitive impairment in humans

Published
2021
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2. 3,4-Dimethoxychalcone induces autophagy through activation of the transcription factors TFE3 and TFEB

Author

Chen, Guo, Xie, Wei, Nah, Jihoon, Sauvat, Allan, Liu, Peng, Pietrocola, Federico, Sica, Valentina, Carmona-Gutierrez, Didac, Zimmermann, Andreas, Pendl, Tobias, Tadic, Jelena, Bergmann, Martina, Hofer, Sebastian, Domuz, Lana, Lachkar, Sylvie, Markaki, Maria, Tavernarakis, Nektarios, Sadoshima, Junichi, Madeo, Frank, Kepp, Oliver, Kroemer, Guido, Apoptose, cancer et immunité (Equipe labellisée Ligue contre le cancer - CRC - Inserm U1138), Institut Gustave Roussy (IGR)-Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), Institut Gustave Roussy (IGR), Sorbonne Université (SU), Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), Université Paris-Saclay, Rutgers New Jersey Medical School (NJMS), Rutgers University System (Rutgers), Karl-Franzens-Universität [Graz, Autriche], University of Novi Sad, Foundation for Research and Technology - Hellas (FORTH), University of Crete [Heraklion] (UOC), École pratique des hautes études (EPHE)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-École pratique des hautes études (EPHE)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), École pratique des hautes études (EPHE)-Université Paris Diderot - Paris 7 (UPD7)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU), and University of Graz

Subjects
Medicine (General), Cardiotonic Agents, Transcription, Genetic, [SDV]Life Sciences [q-bio], [SDV.CAN]Life Sciences [q-bio]/Cancer, QH426-470, Cardiovascular System, Article, Cell Line, Mice, R5-920, Chalcones, Chemical Biology, Medicine and Health Sciences, Genetics, Autophagy, Animals, Humans, Myocytes, Cardiac, Pharmacology & Drug Discovery, Cancer, TFEB, Basic Helix-Loop-Helix Leucine Zipper Transcription Factors, TFEB Subject Categories Cancer, Biology and Life Sciences, Animal Structures, Acetylation, Articles, TFE3, Protein Transport, cardioprotection, Hepatocytes, caloric restriction, caloric restriction mimetic, Protein Processing, Post-Translational, Transcription Factors
Abstract

International audience; Caloric restriction mimetics (CRMs) are natural or synthetic compounds that mimic the health-promoting and longevity-extending effects of caloric restriction. CRMs provoke the deacetylation of cellular proteins coupled to an increase in autophagic flux in the absence of toxicity. Here, we report the identification of a novel candidate CRM, namely 3,4-dimethoxychalcone (3,4-DC), among a library of polyphenols. When added to several different human cell lines, 3,4-DC induced the deacetylation of cytoplasmic proteins and stimulated autophagic flux. At difference with other well-characterized CRMs, 3,4-DC, however, required transcription factor EB (TFEB)- and E3 (TFE3)-dependent gene transcription and mRNA translation to trigger autophagy. 3,4-DC stimulated the translocation of TFEB and TFE3 into nuclei both in vitro and in vivo, in hepatocytes and cardiomyocytes. 3,4-DC induced autophagy in vitro and in mouse organs, mediated autophagy-dependent cardioprotective effects, and improved the efficacy of anticancer chemotherapy in vivo. Altogether, our results suggest that 3,4-DC is a novel CRM with a previously unrecognized mode of action.

Published
2019
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3. Cardioprotection and lifespan extension by the natural polyamine spermidine

Author

Eisenberg, Tobias, Abdellatif, Mahmoud, Zimmermann, Andreas, Schroeder, Sabrina, Pendl, Tobias, Harger, Alexandra, Stekovic, Slaven, Schipke, Julia, Magnes, Christoph, Schmidt, Albrecht, Ruckenstuhl, Christoph, Dammbrueck, Christopher, Gross, Angelina S., Herbst, Viktoria, Carmona-Gutierrez, Didac, Pietrocola, Federico, Pieber, Thomas R., Sigrist, Stephan J., Linke, Wolfgang A., Mühlfeld, Christian, Sadoshima, Junichi, Dengjel, Joern, Kiechl, Stefan, Kroemer, Guido, Sedej, Simon, and Madeo, Frank

Subjects
Mice, Inbred C57BL, autophagy, hypertension, Rats, Inbred Dahl, cardiovascular disease, polyamine, Spermidine, aging, Animals, Humans, Models, Biological, Autophagic Puncta
Abstract

Loss of cardiac macroautophagy/autophagy impairs heart function, and evidence accumulates that an increased autophagic flux may protect against cardiovascular disease. We therefore tested the protective capacity of the natural autophagy inducer spermidine in animal models of aging and hypertension, which both represent major risk factors for the development of cardiovascular disease. Dietary spermidine elicits cardioprotective effects in aged mice through enhancing cardiac autophagy and mitophagy. In salt-sensitive rats, spermidine supplementation also delays the development of hypertensive heart disease, coinciding with reduced arterial blood pressure. The high blood pressure-lowering effect likely results from improved global arginine bioavailability and protection from hypertension-associated renal damage. The polyamine spermidine is naturally present in human diets, though to a varying amount depending on food type and preparation. In humans, high dietary spermidine intake correlates with reduced blood pressure and decreased risk of cardiovascular disease and related death. Altogether, spermidine represents a cardio- and vascular-protective autophagy inducer that can be readily integrated in common diets.

Published
2017

4. Fine-Tuning Cardiac Insulin-Like Growth Factor 1 Receptor Signaling to Promote Health and Longevity.

Author

Abdellatif, Mahmoud, Trummer-Herbst, Viktoria, Heberle, Alexander Martin, Humnig, Alina, Pendl, Tobias, Durand, Sylvère, Cerrato, Giulia, Hofer, Sebastian J., Islam, Moydul, Voglhuber, Julia, Ramos Pittol, José Miguel, Kepp, Oliver, Hoefler, Gerald, Schmidt, Albrecht, Rainer, Peter P., Scherr, Daniel, von Lewinski, Dirk, Bisping, Egbert, McMullen, Julie R., and Diwan, Abhinav

Subjects
*SOMATOMEDIN C, *INSULIN-like growth factor receptors, *LONGEVITY, *CELLULAR aging, *AGING, *EPIDERMAL growth factor receptors, *PHOSPHATIDYLINOSITOL 3-kinases, *CELL metabolism, *SOMATOMEDIN, *PHOSPHOTRANSFERASES, *ANIMAL experimentation, *RESEARCH funding, *HEALTH promotion, *MICE, *ANIMALS
Abstract

Background: The insulin-like growth factor 1 (IGF1) pathway is a key regulator of cellular metabolism and aging. Although its inhibition promotes longevity across species, the effect of attenuated IGF1 signaling on cardiac aging remains controversial.Methods: We performed a lifelong study to assess cardiac health and lifespan in 2 cardiomyocyte-specific transgenic mouse models with enhanced versus reduced IGF1 receptor (IGF1R) signaling. Male mice with human IGF1R overexpression or dominant negative phosphoinositide 3-kinase mutation were examined at different life stages by echocardiography, invasive hemodynamics, and treadmill coupled to indirect calorimetry. In vitro assays included cardiac histology, mitochondrial respiration, ATP synthesis, autophagic flux, and targeted metabolome profiling, and immunoblots of key IGF1R downstream targets in mouse and human explanted failing and nonfailing hearts, as well.Results: Young mice with increased IGF1R signaling exhibited superior cardiac function that progressively declined with aging in an accelerated fashion compared with wild-type animals, resulting in heart failure and a reduced lifespan. In contrast, mice with low cardiac IGF1R signaling exhibited inferior cardiac function early in life, but superior cardiac performance during aging, and increased maximum lifespan, as well. Mechanistically, the late-life detrimental effects of IGF1R activation correlated with suppressed autophagic flux and impaired oxidative phosphorylation in the heart. Low IGF1R activity consistently improved myocardial bioenergetics and function of the aging heart in an autophagy-dependent manner. In humans, failing hearts, but not those with compensated hypertrophy, displayed exaggerated IGF1R expression and signaling activity.Conclusions: Our findings indicate that the relationship between IGF1R signaling and cardiac health is not linear, but rather biphasic. Hence, pharmacological inhibitors of the IGF1 pathway, albeit unsuitable for young individuals, might be worth considering in older adults. [ABSTRACT FROM AUTHOR]

Published
2022
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