EPISODE · May 29, 2026 · 22 MIN
1048-生酮与铁死亡轴维持白血病干细胞存活
from 聊聊Sci
该研究揭示了急性髓系白血病（AML）中一种此前未知的代谢机制，即白血病干细胞（LSCs）通过增强脂肪酸氧化（FAO）实现自主酮体生成。研究发现，关键限速酶 HMGCS2 在白血病干细胞中呈高表达态势，其产生的酮体 BHB 并非仅作为能量来源，而是通过表观遗传方式抑制 FADS2 基因的表达。这种调控减少了促铁死亡磷脂的积累，从而使癌变干细胞免于铁死亡并维持其自我更新能力。实验证明，靶向阻断这一酮生成-铁死亡轴能显著抑制白血病进展，且不会损害正常的造血干细胞。这一发现为开发特异性清除恶性干细胞而不产生系统毒性的精准疗法提供了重要靶点。References:Han X, Wang K, Ma W, et al. A ketogenesis-ferroptosis axis maintains leukemic stem cell survival and leukemia progression[J]. Cell Stem Cell, 2026.前往小宇宙评论区与主播互动
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1048-生酮与铁死亡轴维持白血病干细胞存活
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