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骨髓脂肪细胞在心肌梗塞后的紧急血液形成中提供燃料

Shuang Zhang^1,2, Alexandre Paccalet^1,2, David Rohde^1,2

¹Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA.

Nature cardiovascular research

|February 12, 2024

概括

心脏病发作引发紧急血液细胞的产生,增加心力衰竭的风险. 脂肪酸代谢推动了这一过程,为心血管疾病提供了一个新的治疗点.

科学领域:

心血管生物学心血管生物学
血液形成血液形成血液形成
代谢调节代谢调节代谢调节代谢调节

背景情况:

心肌梗塞 (MI) 诱导紧急血液形成,产生炎症性髓状细胞,使动脉样硬化和心力衰竭恶化.
代谢途径,特别是糖解和线粒体代谢之间的平衡,对于造血干细胞恒温至关重要.

研究的目的:

调查代谢线索,特别是脂肪酸代谢在调节心肌梗塞后的紧急血液形成中的作用.
为了确定潜在的治疗点,以减轻不良后MI造血.

主要方法:

对人类和MI后雌性小鼠的造血原生细胞的分析.
在小鼠 (Vav1-Cpt1Afl/fl,Adipoq-Atgl,Adipoq-2iDTR) 中进行基因操纵,以阻止脂肪酸氧化和脂解.
评估骨髓脂肪和造血细胞群的评估.
药理和手术共感切除术是为了研究同情神经系统的作用.

主要成果:

造血原生细胞在MI后表现出脂肪酸代谢的增加.
在造血细胞中删除卡尼丁棕基转移酶1A (Cpt1A) 降低了MI后的祖细胞增殖和骨髓扩张.
在人类,猪和小鼠中,MI导致骨髓脂肪减少.
抑制脂解或耗尽骨髓脂肪细胞缩短了紧急血液形成.
交感切除术防止了骨髓脂肪细胞在MI后的收缩.

结论:

脂肪酸代谢是心肌梗塞后紧急血液形成的关键调节者.
针对脂肪酸代谢和骨髓脂肪细胞功能,为MI后并发症提供了一个新的治疗策略.

关键词:

心肌梗塞的心脏病发作脂肪细胞 (adipocytes) 是一种脂肪细胞.骨髓骨髓骨髓骨髓骨髓紧急血液形成 (Hematopoiesis) 是一种脂肪酸氧化过程中的脂肪酸氧化.脂肪溶解是指脂质分解的过程.

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