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• W2889010653 abstract "In mammalians, advancing age is associated with sarcopenia, the progressive and involuntary loss of muscle mass and strength. Hyperphosphatemia is an aging-related condition involved in several pathologies. The aim of this work was to assess whether hyperphosphatemia plays a role in the age-related loss of mass muscle and strength by inducing cellular senescence in murine myoblasts and to explore the intracellular mechanism involved in this effect. Cultured mouse C2C12 cells were treated with 10 mM beta-glycerophosphate (BGP] at different periods of time to induce hyperphosphatemia. BGP promoted cellular senescence after 24 h of treatment, assessed by the increased expression of p53, acetylated-p53 and p21 and senescence associated β-galactosidase activity. In parallel, BGP increased ILK expression and activity, followed by mTOR activation and autophagy reduction. Knocking-down ILK expression increased autophagy and protected cells from senescence induced by hyperphosphatemia. BGP also reduced the proliferative capacity of cultured myoblasts. Old mice (24-months-old] presented higher serum phosphate concentration, lower forelimb strength, higher expression of p53 and ILK and less autophagy in vastus muscle than young mice (5-months-old]. In conclusion, we propose that hyperphosphatemia induces senescence in cultured myoblasts through ILK overexpression, reducing their proliferative capacity, which could be a mechanism involved in the development of sarcopenia, since old mice showed loss of muscular strength correlated with high serum phosphate concentration and increased levels of ILK and p53." @default.
• W2889010653 created "2018-09-07" @default.
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• W2889010653 date "2018-01-01" @default.
• W2889010653 modified "2023-10-18" @default.
• W2889010653 title "Hyperphosphatemia Promotes Senescence of Myoblasts by Impairing Autophagy Through Ilk Overexpression, A Possible Mechanism Involved in Sarcopenia" @default.
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• W2889010653 cites W1970204106 @default.
• W2889010653 cites W1978990590 @default.
• W2889010653 cites W1979765208 @default.
• W2889010653 cites W2002435993 @default.
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• W2889010653 cites W2004314923 @default.
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• W2889010653 cites W2008678562 @default.
• W2889010653 cites W2010871579 @default.
• W2889010653 cites W2018876830 @default.
• W2889010653 cites W2022487205 @default.
• W2889010653 cites W2025170983 @default.
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• W2889010653 doi "https://doi.org/10.14336/ad.2017.1214" @default.
• W2889010653 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6147593" @default.
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