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These results indicate that the metabolic shift from glucose substrate-dependent pathway to FAO or glutaminolysis was induced under the exposure to H 2 O 2 regarding the mitochondrial damage, whereas the promotion was not enough to compensate respiratory capacity decrease and was rather a marker of H 2 O 2 -exposed stress, and this shift was held to the nearly normal state with PQQ pretreatment protection

Moreover, the competitive consumption of glutamine by tumor cells, along with the release of its metabolites, profoundly influences immune cells and stromal cells within the TME

Amphipathic lipid metabolites and their relation to arrhythmogenesis in the ischemic heart

34, Aug

[DOI] [PubMed] [Google Scholar] 130.Makhseed N, Vallance HD, Potter M, Waters PJ, Wong LT, Lillquist Y, Pasquali M, Amat di San Filippo C, Longo N