Glycolysis in senescence (Homo sapiens)
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Description
The upregulation of several glycolytic enzymes seems to mediate increased glycolysis in various types of induced senescence. Depending on the stimulus, various proteins and genes influence glycolytic rates. For example, in irradiation-induced senescence, this effect seems to be mediated by AMPK activation and NF-kB signalling (Nacarelli & Sell, 2017). Similarly, in OIS, the retinoblastoma protein appears to upregulate glycolytic genes (Nacarelli & Sell, 2017). The very important p53 is known to be a central mediator of senescence, due to its role in cell cycle regulation. It has been found to negatively affect glycolysis (Gu et al., 2018). However it also has an indirect positive effect on it, by activating G6PDH in stressed cells (Jiang et al., 2011). TP53 is therefore thought to have a regulatory role on glycolysis and is interesting in the context of senescence.
While most glycolytic enzymes are upregulated (Zwerschke et al., 2003), GAPDH seems to decrease. This may partially be explained by the sensitivity of the enzyme to oxidative stress.
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- Birgit Veldman; ''Metabolic hallmarks of cellular senescence: highlighting the role of intracellular pathways in various senescent phenotypes''; Unpublished, 2020
- Wiley CD, Campisi J; ''From Ancient Pathways to Aging Cells-Connecting Metabolism and Cellular Senescence.''; Cell Metab, 2016 PubMed Europe PMC Scholia
- Mazurek S, Zwerschke W, Jansen-Dürr P, Eigenbrodt E; ''Metabolic cooperation between different oncogenes during cell transformation: interaction between activated ras and HPV-16 E7.''; Oncogene, 2001 PubMed Europe PMC Scholia
- Jiang P, Du W, Wang X, Mancuso A, Gao X, Wu M, Yang X; ''p53 regulates biosynthesis through direct inactivation of glucose-6-phosphate dehydrogenase.''; Nat Cell Biol, 2011 PubMed Europe PMC Scholia
- Nacarelli T, Sell C; ''Targeting metabolism in cellular senescence, a role for intervention''; https://doi.org/10.1016/j.mce.2016.08.049, 2017 PubMed Europe PMC Scholia
- Gu J, Wang S, Guo H, Tan Y, Liang Y, Feng A, Liu Q, Damodaran C, Zhang Z, Keller BB, Zhang C, Cai L; ''Inhibition of p53 prevents diabetic cardiomyopathy by preventing early-stage apoptosis and cell senescence, reduced glycolysis, and impaired angiogenesis.''; Cell Death Dis, 2018 PubMed Europe PMC Scholia
- Sabbatinelli J, Prattichizzo F, Olivieri F, Procopio AD, Rippo MR, Giuliani A; ''Where Metabolism Meets Senescence: Focus on Endothelial Cells.''; Front Physiol, 2019 PubMed Europe PMC Scholia
- Dörr JR, Yu Y, Milanovic M, Beuster G, Zasada C, Däbritz JH, Lisec J, Lenze D, Gerhardt A, Schleicher K, Kratzat S, Purfürst B, Walenta S, Mueller-Klieser W, Gräler M, Hummel M, Keller U, Buck AK, Dörken B, Willmitzer L, Reimann M, Kempa S, Lee S, Schmitt CA; ''Synthetic lethal metabolic targeting of cellular senescence in cancer therapy.''; Nature, 2013 PubMed Europe PMC Scholia
- Zwerschke W, Mazurek S, Stöckl P, Hütter E, Eigenbrodt E, Jansen-Dürr P; ''Metabolic analysis of senescent human fibroblasts reveals a role for AMP in cellular senescence.''; Biochem J, 2003 PubMed Europe PMC Scholia
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