吡哆醛-5-磷酸通过H2S/AKT/GSK3β信号轴减轻大鼠心脏年龄相关的代谢失衡。

IF 4.5 3区生物学 Q2 CELL BIOLOGY

Mitochondrion Pub Date : 2025-01-02 DOI:10.1016/j.mito.2024.102001

Nataliia A. Strutynska , Volodymyr V. Balatskyi , Ruslan B. Strutynskyi , Yulia V. Goshovska , Lidiia A. Mys , Alina Yu. Luchkova , Maiia V. Denysova , Yuliia P. Korkach , Vladyslav R. Strutynskyi , Oksana O. Piven , Pawel Dobrzyn , Vadym F. Sagach

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引用次数: 0

摘要

吡哆醛-5-磷酸（PLP）促进内源性硫化氢的合成，硫化氢是细胞代谢的有效调节剂。我们用24月龄大鼠研究PLP对衰老心脏的有丝分裂保护作用。我们证明了PLP给药后线粒体生物能量功能的改善，mPTP开放的抑制。此外，PLP处理增加了葡萄糖的消耗和利用，减少了脂质向细胞的转运，但增加了脂肪酸β-氧化，提供了足够的能量。心电图研究显示，plp治疗的老年大鼠心功能有显著改善。我们的数据表明，PLP可能通过H2S/AKT/GSK3β轴发挥作用，并进一步靶向Sirt1/PGC-1α信号通路。

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Pyridoxal-5-phosphate mitigates age-related metabolic imbalances in the rat heart through the H2S/AKT/GSK3β signaling axis

Pyridoxal-5-phosphate (PLP) enhances the synthesis of endogenous hydrogen sulfide, a potent regulator of cell metabolism. We used 24-month-old rats to investigate the PLP mitoprotective function in the aging heart. We demonstrated improvement of mitochondrial bioenergetic functions, inhibition of mPTP opening after PLP administration. Moreover, PLP treatment increased glucose consumption and utilization, decreased lipid transport into the cells, but increased fatty acid β-oxidation, providing sufficient energy. An ECG study showed a significant improvement in cardiac function in PLP-treated old rats. Our data suggest that PLP may exert its effect through the H₂S/AKT/GSK3β axis with further targeting of the Sirt1/PGC-1α signaling pathway.

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来源期刊

Mitochondrion 生物-细胞生物学

CiteScore

9.40

自引率

4.50%

发文量

审稿时长

13.6 weeks

期刊介绍： Mitochondrion is a definitive, high profile, peer-reviewed international research journal. The scope of Mitochondrion is broad, reporting on basic science of mitochondria from all organisms and from basic research to pathology and clinical aspects of mitochondrial diseases. The journal welcomes original contributions from investigators working in diverse sub-disciplines such as evolution, biophysics, biochemistry, molecular and cell biology, genetics, pharmacology, toxicology, forensic science, programmed cell death, aging, cancer and clinical features of mitochondrial diseases.