Disruption of phosphofructokinase activity and aerobic glycolysis in human bronchial epithelial cells by atmospheric ultrafine particulate matter

Park, Su Hwan; Kim, Gyuri; Yang, Gi-Eun; Yun, Hye Jin; Shin, Tae Hwan; Kim, Sun Tae; Lee, Kyuhong; Kim, Hyuk Soon; Kim, Seok-Ho; Leem, Sun-Hee; Cho, Wan-Seob; Lee, Jong-Ho

doi:10.1016/j.jhazmat.2023.132966

Cited by 2 publications

(2 citation statements)

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“…This research was consistent with previous evidence that the rate of NADH oxidation could limit biomass synthesis in aerobic conditions if proliferation is quick enough, in the context of impaired mitochondrial OXPHOS capacity [46]. This also supports previous proposals on the role of aerobic glycolysis in protecting against oxidative stress in proliferating cells [43].…”

Section: Nad + Demand Driving Aerobic Glycolysissupporting

confidence: 92%

“…However, conflicting data has noted most of the biomass from proliferating cells is derived from amino acids rather than glucose derivatives, which again challenges this notion [42]. Other authors have proposed that aerobic glycolysis may protect against the increased oxidative stress seen in a proliferating cell [43]. Aerobic glycolysis has recently been found to be a rate-limiting factor for the proliferation and survival of human bronchial epithelial cells [44].…”

Section: Aerobic Glycolysismentioning

confidence: 99%

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Metabolic adaption of epithelial cells in asthma: a window to the initiation of carcinogenesis?

Dymond

2024

Explor Asthma Allergy

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Recent data has resulted in an interest in the metabolic shift in cellular metabolism to aerobic glycolysis, increased reactive oxygen species (ROS), and mitochondrial dysfunction associated with asthma. There has been a push to better understand the immune and metabolic changes in allergy to improve understanding of disease pathology and treatment. Aerobic glycolysis seen in epithelial cells in asthma promotes chronic inflammation and the production of inflammatory cytokines. Asthma epithelial cells share a number of features proposed in the stages of cancer initiation including aerobic glycolysis and increased apoptosis with proliferation, all within a chronic inflammatory microenvironment. Metabolic reprogramming in malignant cells has been widely investigated since the glycolytic characteristics were first described last century. It is still debated whether these metabolic changes are the cause or consequence of carcinogenesis and oncogenic cell-selective pressures. Although historic results have been conflicting, recent data has found an increased lung cancer risk in asthma patients, independent of risk factors. A review of emerging research on the metabolic changes seen in asthma helps us to propose a pathway between the initiation of aerobic glycolysis and the selective pressures of the epithelial microenvironment and resulting malignant transformation risk.

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Section: Nad + Demand Driving Aerobic Glycolysissupporting

confidence: 92%