Violeta
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https://www.atsjournals.org/doi/full/10.1164/rccm.202005-1583OC
IL-1β, IL-6, IL-8, and sTNFR1 were all increased in patients with COVID-19
COVID-19 neutrophils displayed altered immunometabolism, with increased cytosolic PKM2 (pyruvate kinase M2), phosphorylated PKM2, HIF-1α (hypoxia-inducible factor-1α), and lactate.
Neutrophils undergo immunometabolic reprogramming in severe COVID-19 illness.
COVID-19 neutrophils displayed altered immunometabolism, with increased cytosolic PKM2 (pyruvate kinase M2), phosphorylated PKM2, HIF-1α (hypoxia-inducible factor-1α), and lactate.
Critical illness is notable for markedly increased energy demands. ATP serves as the building block of this energy and is produced via two linked metabolic pathways, glycolysis and the tricarboxylic acid cycle, also known as Krebs’ cycle. Although quiescent human neutrophils demonstrate tricarboxylic acid cycle activity, their metabolism is predominantly glycolytic. Certain circumstances, such as hypoxemia, infection, and inflammation, stand to shift the metabolism of circulating neutrophils further toward glycolysis.
PKM2, on the other hand, displays lower enzymatic activity than PKM1, and instead promotes increased glycolysis with resultant cytosolic accumulation of lactate and other metabolic intermediates (5). PKM2 can assume different conformations, with dimers existing in equilibrium with tetramers. Critically, PKM2 dimers are capable of nuclear translocation, where they directly interact with the transcription factor HIF-1α (hypoxia-inducible factor-1α.
The most interesting thing about this article is the relationship between PKM2 and ME/CFS.
PKM2 accelerated the progressionof chronic fatigue syndrome viapromoting the H4K12la/ NF-κB induced neuroinflammation andmitochondrial damage
https://www.nature.com/articles/s41598-025-93313-w.pdf
IL-1β, IL-6, IL-8, and sTNFR1 were all increased in patients with COVID-19
COVID-19 neutrophils displayed altered immunometabolism, with increased cytosolic PKM2 (pyruvate kinase M2), phosphorylated PKM2, HIF-1α (hypoxia-inducible factor-1α), and lactate.
Neutrophils undergo immunometabolic reprogramming in severe COVID-19 illness.
COVID-19 neutrophils displayed altered immunometabolism, with increased cytosolic PKM2 (pyruvate kinase M2), phosphorylated PKM2, HIF-1α (hypoxia-inducible factor-1α), and lactate.
Critical illness is notable for markedly increased energy demands. ATP serves as the building block of this energy and is produced via two linked metabolic pathways, glycolysis and the tricarboxylic acid cycle, also known as Krebs’ cycle. Although quiescent human neutrophils demonstrate tricarboxylic acid cycle activity, their metabolism is predominantly glycolytic. Certain circumstances, such as hypoxemia, infection, and inflammation, stand to shift the metabolism of circulating neutrophils further toward glycolysis.
PKM2, on the other hand, displays lower enzymatic activity than PKM1, and instead promotes increased glycolysis with resultant cytosolic accumulation of lactate and other metabolic intermediates (5). PKM2 can assume different conformations, with dimers existing in equilibrium with tetramers. Critically, PKM2 dimers are capable of nuclear translocation, where they directly interact with the transcription factor HIF-1α (hypoxia-inducible factor-1α.
The most interesting thing about this article is the relationship between PKM2 and ME/CFS.
PKM2 accelerated the progressionof chronic fatigue syndrome viapromoting the H4K12la/ NF-κB induced neuroinflammation andmitochondrial damage
https://www.nature.com/articles/s41598-025-93313-w.pdf