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转硫化通路的激活减轻了状初级红细胞和转基因小鼠的氧化应激和铁亡

Caixia Xi^1,2, Junfeng Pang¹, Weinan Xue¹

¹Georgia Cancer Center, Augusta University, Augusta, GA, 30912, USA.

Communications biology

|January 6, 2025

概括

转硫化途径支持状细胞病 (SCD) 中的氨酸水平. 使用二甲基烟酸 (DMF) 激活囊氨酸β-合成酶 (CBS),可增强谷氨酸的活性,防止SCD中的氧化应激和铁.

科学领域:

生物化学生物化学
细胞生物学细胞生物学
血液学血液学血液学

背景情况:

转硫 (TSS) 途径是氨酸合成的氨酸的关键来源.
在状细胞疾病 (SCD) 中,TSS通路的抗氧化作用尚不清楚.
半氨酸的可用性对于减轻SCD中氧化应激和铁亡是至关重要的.

研究的目的:

调查TSS途径,特别是cystathionine beta-synthase (CBS) 在SCD中控制氧化应激和铁亡的作用.
评估激活TSS途径作为SCD治疗策略的潜力.

主要方法:

在不同条件下 (血红素暴露,囊素补充) 评估TSS途径对囊素水平的贡献.
研究了CBS表达的调节机制,包括黑的抑制作用和通过NRF2的二甲基烟酸 (DMF) 的诱导作用.
分析了DMF诱导的DNA基甲基化对CBS基因表达和染色质结构的影响.

主要成果:

TSS途径对囊素供应至关重要,特别是在半膜应激或囊素有限的情况下.
血抑制了CBS的表达,抑制了TSS途径和新型囊蛋白合成.
甲基二醇烟酸 (DMF) 通过NRF2激活和增加DNA基甲基化来提高CBS表达的调节,从而提高谷氨水平.

结论:

通过TSS通路激活CBS对于在特定压力条件下维持SCD中的囊类平衡至关重要.
由DMF诱导的CBS上调会增加细胞谷氨,对SCD中反应性氧物种 (ROS) 和铁死提供保护.
准TSS途径为管理状细胞疾病中氧化损伤提供了潜在的治疗途径.

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