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2004;134(6 Suppl):1575S82S

[DOI] [PMC free article] [PubMed] [Google Scholar] 130

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At subtoxic concentrations, H 2 S has been shown to stimulate ATP production at the level of oxidative phosphorylation, both as a source of electron equivalents for the mETC (via SQR-mediated quinone reduction, Table 1), and through per-sulphidation of ATPase, which maintains the enzyme in its activated state

Accordingly, p300/CBP, LDH and MCTs are best viewed as clinically druggable entry points into the lactatelactylation axis rather than lactylation-specific drug targets: p300/CBP are pleiotropic co-activators that write multiple acyl-lysine marks, LDH inhibition alters redox balance and central carbon flux, and MCT blockade reshapes extracellular acidity and metabolite exchange across tumor and immune compartments [23, 48, 124, 316, 317]