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10.3390/v14050983

http://scihub22266oqcxt.onion/10.3390/v14050983
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35632725!9143006!35632725
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suck abstract from ncbi


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pmid35632725      Viruses 2022 ; 14 (5): ä
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  • SARS-CoV-2 Causes Lung Inflammation through Metabolic Reprogramming and RAGE #MMPMID35632725
  • Allen CNS; Santerre M; Arjona SP; Ghaleb LJ; Herzi M; Llewellyn MD; Shcherbik N; Sawaya BE
  • Viruses 2022[May]; 14 (5): ä PMID35632725show ga
  • Clinical studies indicate that patients infected with SARS-CoV-2 develop hyperinflammation, which correlates with increased mortality. The SARS-CoV-2/COVID-19-dependent inflammation is thought to occur via increased cytokine production and hyperactivity of RAGE in several cell types, a phenomenon observed for other disorders and diseases. Metabolic reprogramming has been shown to contribute to inflammation and is considered a hallmark of cancer, neurodegenerative diseases, and viral infections. Malfunctioning glycolysis, which normally aims to convert glucose into pyruvate, leads to the accumulation of advanced glycation end products (AGEs). Being aberrantly generated, AGEs then bind to their receptor, RAGE, and activate several pro-inflammatory genes, such as IL-1b and IL-6, thus, increasing hypoxia and inducing senescence. Using the lung epithelial cell (BEAS-2B) line, we demonstrated that SARS-CoV-2 proteins reprogram the cellular metabolism and increase pyruvate kinase muscle isoform 2 (PKM2). This deregulation promotes the accumulation of AGEs and senescence induction. We showed the ability of the PKM2 stabilizer, Tepp-46, to reverse the observed glycolysis changes/alterations and restore this essential metabolic process.
  • |*COVID-19[MESH]
  • |*Pneumonia[MESH]
  • |Humans[MESH]
  • |Inflammation[MESH]
  • |Pyridazines[MESH]
  • |Pyrroles[MESH]


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