Trichostatin A improved dendritic cell function by enhancing glycolysis and modulating metabolism via PKM2 during oxygen-glucose deprivation conditions.
Does Trichostatin A alleviate oxygen-glucose deprivation-induced cellular damage in dendritic cells?
Trichostatin A protects dendritic cells from ischemic damage by regulating glucose and lipid metabolism through PKM2, highlighting a potential therapeutic target for immune modulation in myocardial infarction.
Dendritic cells (DCs) play a crucial role in immune protection against myocardial infarction (MI). Through multiple experimental methods including bioinformatics, qPCR, Western blotting, immunofluorescence, MTT assays, echocardiography, TTC staining, and flow cytometry, this study found that metabolism was demonstrated to be markedly altered under oxygen–glucose deprivation (OGD) conditions in DCs. Pyruvate kinase M2 (PKM2) is a key protein in metabolism, and PKM2 was upregulated under OGD conditions in DCs. Trichostatin A (TSA) alleviated the OGD-induced cellular damage in DCs. Furthermore, TSA was shown to modulate DCs’ function by enhancing glycolysis while suppressing fatty acid synthesis and oxidation pathways. The metabolic changes caused by TSA and OGD were mechanistically mediated by PKM2. Mechanistically, PKM2 modulates glucose and lipid metabolism via its dimer formation. These results deepen our understanding of the interplay among TSA, glucose and lipid metabolism and DC functions in MI.
Yang et al. (2026) studied this question. Trichostatin A improved dendritic cell function by enhancing glycolysis and modulating metabolism via PKM2 during oxygen-glucose deprivation conditions.