Persistent enhancement of glycolysis in kidney tubular epithelial cells has been linked to the progression of chronic kidney disease, although the underlying mechanisms are largely unknown. In this issue of Kidney International, Wang et al. report that the glycolytic enzyme 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 plays a crucial role in kidney fibrosis by enhancing histone H4 lysine 12 lactylation through lactate accumulation. This increases the transcription of nuclear factor-κB–related genes and promotes inflammation and fibrosis. Inhibiting 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase 3 reduces these effects, indicating therapeutic potential for kidney fibrosis.

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乳酸：CKD 进展中代谢和炎症之间缺失的环节？


肾小管上皮细胞糖酵解的持续增强与慢性肾病的进展有关，但其潜在机制在很大程度上尚不清楚。在本期 Kidney International 中，Wang 等 人报道了糖酵解酶 6-磷酸果糖-2-激酶/果糖-2,6-二磷酸酶 3 通过乳酸积累增强组蛋白 H4 赖氨酸 12 乳酸化，在肾纤维化中起着至关重要的作用。这增加了核因子-κB 相关基因的转录，并促进了炎症和纤维化。抑制 6-磷酸果糖-2-激酶/果糖-2,6-二磷酸酶 3 可降低这些作用，表明肾纤维化具有治疗潜力。