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Key regulatory axes—including HIF-1α, HHIP-PKM2, PTGES-AKT-HIF-1α, and lactate/LDH-A (LDH5)-TGF-β—interact to collectively promote enhanced glycolysis and diminished oxidative metabolism, sustaining the pathological phenotype of the disease ( Abnormalities in the PPP are primarily manifested as oxidative stress-induced compensatory activation