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18 results on '"Hsu, Myriam Y."'

1. NAD+ repletion with niacin counteracts cancer cachexia

Author

Beltrà, Marc, Pöllänen, Noora, Fornelli, Claudia, Tonttila, Kialiina, Hsu, Myriam Y., Zampieri, Sandra, Moletta, Lucia, Corrà, Samantha, Porporato, Paolo E., Kivelä, Riikka, Viscomi, Carlo, Sandri, Marco, Hulmi, Juha J., Sartori, Roberta, Pirinen, Eija, and Penna, Fabio

Published
2023
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2. Iron supplementation is sufficient to rescue skeletal muscle mass and function in cancer cachexia

Author

Wyart, Elisabeth, Hsu, Myriam Y, Sartori, Roberta, Mina, Erica, Rausch, Valentina, Pierobon, Elisa S, Mezzanotte, Mariarosa, Pezzini, Camilla, Bindels, Laure B, Lauria, Andrea, Penna, Fabio, Hirsch, Emilio, Martini, Miriam, Mazzone, Massimiliano, Roetto, Antonella, Geninatti Crich, Simonetta, Prenen, Hans, Sandri, Marco, Menga, Alessio, and Porporato, Paolo E

Published
2022
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4. Flvcr1a deficiency promotes heme-based energy metabolism dysfunction in skeletal muscle

Author

Mistretta, Miriam, primary, Fiorito, Veronica, additional, Allocco, Anna Lucia, additional, Ammirata, Giorgia, additional, Hsu, Myriam Y., additional, Digiovanni, Sabrina, additional, Belicchi, Marzia, additional, Napoli, Laura, additional, Ripolone, Michela, additional, Trombetta, Elena, additional, Mauri, PierLuigi, additional, Farini, Andrea, additional, Meregalli, Mirella, additional, Villa, Chiara, additional, Porporato, Paolo Ettore, additional, Miniscalco, Barbara, additional, Crich, Simonetta Geninatti, additional, Riganti, Chiara, additional, Torrente, Yvan, additional, and Tolosano, Emanuela, additional

Published
2024
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5. FK506 bypasses the effect of erythroferrone in cancer cachexia skeletal muscle atrophy

Author

Mina, Erica, primary, Wyart, Elisabeth, additional, Sartori, Roberta, additional, Angelino, Elia, additional, Zaggia, Ivan, additional, Rausch, Valentina, additional, Maldotti, Mara, additional, Pagani, Alessia, additional, Hsu, Myriam Y., additional, Friziero, Alberto, additional, Sperti, Cosimo, additional, Menga, Alessio, additional, Graziani, Andrea, additional, Hirsch, Emilio, additional, Oliviero, Salvatore, additional, Sandri, Marco, additional, Conti, Laura, additional, Kautz, Léon, additional, Silvestri, Laura, additional, and Porporato, Paolo E., additional

Published
2023
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9. NAD+ repletion with niacin counteracts cancer cachexia

Author

Beltrà, Marc, primary, Pöllänen, Noora, additional, Fornelli, Claudia, additional, Tonttila, Kialiina, additional, Hsu, Myriam Y., additional, Zampieri, Sandra, additional, Moletta, Lucia, additional, Porporato, Paolo E., additional, Kivelä, Riikka, additional, Sandri, Marco, additional, Hulmi, Juha J., additional, Sartori, Roberta, additional, Pirinen, Eija, additional, and Penna, Fabio, additional

Published
2022
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10. Iron supplementation is sufficient to rescue skeletal muscle mass and function in cancer cachexia.

Author

UCL - SSS/LDRI - Louvain Drug Research Institute, Wyart, Elisabeth, Hsu, Myriam Y, Sartori, Roberta, Mina, Erica, Rausch, Valentina, Pierobon, Elisa S, Mezzanotte, Mariarosa, Pezzini, Camilla, Bindels, Laure B., Lauria, Andrea, Penna, Fabio, Hirsch, Emilio, Martini, Miriam, Mazzone, Massimiliano, Roetto, Antonella, Geninatti Crich, Simonetta, Prenen, Hans, Sandri, Marco, Menga, Alessio, Porporato, Paolo E, UCL - SSS/LDRI - Louvain Drug Research Institute, Wyart, Elisabeth, Hsu, Myriam Y, Sartori, Roberta, Mina, Erica, Rausch, Valentina, Pierobon, Elisa S, Mezzanotte, Mariarosa, Pezzini, Camilla, Bindels, Laure B., Lauria, Andrea, Penna, Fabio, Hirsch, Emilio, Martini, Miriam, Mazzone, Massimiliano, Roetto, Antonella, Geninatti Crich, Simonetta, Prenen, Hans, Sandri, Marco, Menga, Alessio, and Porporato, Paolo E

Abstract

Cachexia is a wasting syndrome characterized by devastating skeletal muscle atrophy that dramatically increases mortality in various diseases, most notably in cancer patients with a penetrance of up to 80%. Knowledge regarding the mechanism of cancer-induced cachexia remains very scarce, making cachexia an unmet medical need. In this study, we discovered strong alterations of iron metabolism in the skeletal muscle of both cancer patients and tumor-bearing mice, characterized by decreased iron availability in mitochondria. We found that modulation of iron levels directly influences myotube size in vitro and muscle mass in otherwise healthy mice. Furthermore, iron supplementation was sufficient to preserve both muscle function and mass, prolong survival in tumor-bearing mice, and even rescues strength in human subjects within an unexpectedly short time frame. Importantly, iron supplementation refuels mitochondrial oxidative metabolism and energy production. Overall, our findings provide new mechanistic insights in cancer-induced skeletal muscle wasting, and support targeting iron metabolism as a potential therapeutic option for muscle wasting diseases.

Published
2022

11. NAD+ repletion with niacin counteracts cancer cachexia.

Author

Beltrà, Marc, Pöllänen, Noora, Fornelli, Claudia, Tonttila, Kialiina, Hsu, Myriam Y., Zampieri, Sandra, Moletta, Lucia, Corrà, Samantha, Porporato, Paolo E., Kivelä, Riikka, Viscomi, Carlo, Sandri, Marco, Hulmi, Juha J., Sartori, Roberta, Pirinen, Eija, and Penna, Fabio

Subjects
NIACIN, NAD (Coenzyme), CACHEXIA, NICOTINAMIDE, WASTING syndrome, ENERGY metabolism, MUSCLE metabolism
Abstract

Cachexia is a debilitating wasting syndrome and highly prevalent comorbidity in cancer patients. It manifests especially with energy and mitochondrial metabolism aberrations that promote tissue wasting. We recently identified nicotinamide adenine dinucleotide (NAD+) loss to associate with muscle mitochondrial dysfunction in cancer hosts. In this study we confirm that depletion of NAD+ and downregulation of Nrk2, an NAD+ biosynthetic enzyme, are common features of severe cachexia in different mouse models. Testing NAD+ repletion therapy in cachectic mice reveals that NAD+ precursor, vitamin B3 niacin, efficiently corrects tissue NAD+ levels, improves mitochondrial metabolism and ameliorates cancer- and chemotherapy-induced cachexia. In a clinical setting, we show that muscle NRK2 is downregulated in cancer patients. The low expression of NRK2 correlates with metabolic abnormalities underscoring the significance of NAD+ in the pathophysiology of human cancer cachexia. Overall, our results propose NAD+ metabolism as a therapy target for cachectic cancer patients. The loss of nicotinamide adenine dinucleotide is reported to be associated with muscle mitochondrial dysfunction in murine cancer models. Here the authors show that niacin supplementation improves mitochondrial metabolism and reduces muscle wasting in mouse models of cachexia. [ABSTRACT FROM AUTHOR]

Published
2023
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12. Phosphoinositide Conversion Inactivates R‐RAS and Drives Metastases in Breast Cancer

Author

Li, Huayi, primary, Prever, Lorenzo, additional, Hsu, Myriam Y., additional, Lo, Wen‐Ting, additional, Margaria, Jean Piero, additional, De Santis, Maria Chiara, additional, Zanini, Cristina, additional, Forni, Marco, additional, Novelli, Francesco, additional, Pece, Salvatore, additional, Di Fiore, Pier Paolo, additional, Porporato, Paolo Ettore, additional, Martini, Miriam, additional, Belabed, Hassane, additional, Nazare, Marc, additional, Haucke, Volker, additional, Gulluni, Federico, additional, and Hirsch, Emilio, additional

Published
2022
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17. Flvcr1adeficiency promotes heme-based energy metabolism dysfunction in skeletal muscle

Author

Mistretta, Miriam, Fiorito, Veronica, Allocco, Anna Lucia, Ammirata, Giorgia, Hsu, Myriam Y., Digiovanni, Sabrina, Belicchi, Marzia, Napoli, Laura, Ripolone, Michela, Trombetta, Elena, Mauri, PierLuigi, Farini, Andrea, Meregalli, Mirella, Villa, Chiara, Porporato, Paolo Ettore, Miniscalco, Barbara, Crich, Simonetta Geninatti, Riganti, Chiara, Torrente, Yvan, and Tolosano, Emanuela

Abstract

The definition of cell metabolic profile is essential to ensure skeletal muscle fiber heterogeneity and to achieve a proper equilibrium between the self-renewal and commitment of satellite stem cells. Heme sustains several biological functions, including processes profoundly implicated with cell metabolism. The skeletal muscle is a significant heme-producing body compartment, but the consequences of impaired heme homeostasis on this tissue have been poorly investigated. Here, we generate a skeletal-muscle-specific feline leukemia virus subgroup C receptor 1a (FLVCR1a) knockout mouse model and show that, by sustaining heme synthesis, FLVCR1a contributes to determine the energy phenotype in skeletal muscle cells and to modulate satellite cell differentiation and muscle regeneration.

Published
2024
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18. Assessing Metabolic Dysregulation in Muscle During Cachexia.

Author

Hsu MY, Porporato PE, and Wyart E

Subjects
Humans, Mitochondria metabolism, Muscle Fibers, Skeletal metabolism, Muscle, Skeletal pathology, Muscular Atrophy, Neoplasms metabolism, Oxygen metabolism, Cachexia etiology, Cachexia metabolism, Energy Metabolism, Muscle, Skeletal metabolism, Neoplasms complications
Abstract

Cancer cachexia is a metabolic disease characterized by a negative energy balance associated with systemic weight loss and poor quality of life.In particular, skeletal muscle, which represents almost 50% of the total body mass, is strongly affected, and metabolic alterations therein (e.g., insulin resistance and mitochondrial dysfunction) can eventually support tumor growth by facilitating nutrient scavenging by the growing mass. Interestingly, metabolic interventions on wasting muscle have been proven to be protective, advocating for the importance of metabolic regulation in the wasting muscle.Here, we will briefly define the current knowledge of metabolic regulation in cachexia and provide a protocol to grow and differentiate in vitro myotubes for the assessment of mitochondrial metabolism during cachexia.

Published
2019
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