Department of Bioregulatory Science, Graduate School of Medicine, Nippon Medical School, Tokyo, Japan.
Department of Clinical Cancer Genomics, International Medical Center, Saitama Medical University, Saitama, Japan.
J Cardiovasc Pharmacol. 2024 May 1;83(5):433-445. doi: 10.1097/FJC.0000000000001552.
We previously reported a novel compound called S-nitroso- N -pivaloyl- d -penicillamine (SNPiP), which was screened from a group of nitric oxide donor compounds with a basic chemical structure of S-nitroso- N -acetylpenicillamine, to activate the nonneuronal acetylcholine system. SNPiP-treated mice exhibited improved cardiac output and enhanced diastolic function, without an increase in heart rate. The nonneuronal acetylcholine-activating effects included increased resilience to ischemia, modulation of energy metabolism preference, and activation of angiogenesis. Here, we performed transcriptome analysis of SNPiP-treated mice ventricles to elucidate how SNPiP exerts beneficial effects on cardiac function. A time-course study (24 and 48 hours after SNPiP administration) revealed that SNPiP initially induced Wnt and cyclic guanosine monophosphate-protein kinase G signaling pathways, along with upregulation of genes involved in cardiac muscle tissue development and oxytocin signaling pathway. We also observed enrichment of glycolysis-related genes in response to SNPiP treatment, resulting in a metabolic shift from oxidative phosphorylation to glycolysis, which was suggested by reduced cardiac glucose contents while maintaining adenosine tri-phosphate levels. In addition, SNPiP significantly upregulated atrial natriuretic peptide and sarcolipin, which play crucial roles in calcium handling and cardiac performance. These findings suggest that SNPiP may have therapeutic potential based on the pleiotropic mechanisms elucidated in this study.
我们之前报道了一种名为 S-亚硝基-N-戊酰-D-青霉胺(SNPiP)的新型化合物,它是从一组具有 S-亚硝基-N-乙酰青霉胺基本化学结构的一氧化氮供体化合物中筛选出来的,用于激活非神经元乙酰胆碱系统。SNPiP 处理的小鼠表现出改善的心输出量和增强的舒张功能,而心率没有增加。非神经元乙酰胆碱激活作用包括增加对缺血的抵抗力、调节能量代谢偏好和激活血管生成。在这里,我们对 SNPiP 处理的小鼠心室进行了转录组分析,以阐明 SNPiP 如何对心脏功能产生有益影响。一项时间进程研究(SNPiP 给药后 24 和 48 小时)表明,SNPiP 最初诱导 Wnt 和环鸟苷酸蛋白激酶 G 信号通路,以及涉及心肌组织发育和催产素信号通路的基因上调。我们还观察到对 SNPiP 处理的糖酵解相关基因的富集,导致代谢从氧化磷酸化转向糖酵解,这表现在心脏葡萄糖含量降低而三磷酸腺苷水平保持不变。此外,SNPiP 显著上调了心房利钠肽和肌浆球蛋白,它们在钙处理和心脏功能中发挥关键作用。这些发现表明,SNPiP 可能具有基于本研究阐明的多效机制的治疗潜力。