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纤维细胞到心肌细胞的乳酸穿调节高血压心脏重塑

Tong Wei^1,2, Yuetong Guo¹, Chenglin Huang¹

¹Department of Cardiovascular Medicine, State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.

Cell & bioscience

|August 14, 2023

概括

心脏纤维细胞转移新陈代谢以产生乳酸,为心肌细胞提供燃料. 准GCN5L1-MPC2信号传输和乳酸穿可能会减少高血压中的心脏重塑.

科学领域:

心血管生物学心血管生物学
细胞的新陈代谢
分子心脏病学分子心脏病学

背景情况:

心脏纤维细胞 (CFs) 和心肌细胞是关键的心脏细胞.
CFs支持心肌细胞并影响营养代谢.
建议从CFs到心肌细胞的细胞间乳酸运输,但在机制上尚未探索.

研究的目的:

研究乳酸生成和从CF转移到心肌细胞的机制.
探索特定信号通路和传送器在心脏代谢和重塑中的作用.

主要方法:

ангиотензин II (Ang II) 治疗以诱导CF分化为肌纤维细胞.
分析代谢变化,包括氧化酸化和有氧糖解.
研究了GCN5L1 (一种乙转移酶) 和MPC2 (线粒体中酸盐载体) 的作用.
使用了淘汰赛小鼠模型 (肌纤维细胞特异性GCN5L1淘汰赛和心肌细胞特异性MCT1淘汰赛).

主要成果:

安格II诱导CFs进行有氧糖解,上调GCN5L1的调节,该酸乙烯化MPC2,抑制线粒体的pyruvate吸收和呼吸.
消去GCN5L1可以逆转这些代谢变化,减少糖解和乳酸.
肌纤维细胞特异性GCN5L1淘汰会减少心脏缩和原沉积.
特定于心肌细胞的MCT1敲击阻断了乳酸转移,并减轻了Ang II诱导的心脏缩.

结论:

GCN5L1-MPC2信号通路调节心脏细胞的新陈代谢.
阻断单碳酸盐载体1 (MCT1) 干扰了纤维细胞到心肌细胞的乳酸穿.
针对这些途径可能提供治疗策略,以减轻高血压中的心脏重塑.

关键词:

在GCN5L1中.乳酸转运器乳酸转运器在MCT1中,MCT1是MCT1.在MPC2中,MPC2是MPC2.代谢发生转变.

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