Xie Tao, Zhang Zhen, Feng Mingzhe, Kong Lingbo
Department of Spine Surgery, Xi'an Honghui Hospital, Xi'an Jiaotong University, Xi'an, 710054, China.
Medical College, Yan'an University, Yan'an City, Shaanxi, China.
Mol Biol Rep. 2025 Apr 15;52(1):397. doi: 10.1007/s11033-025-10491-6.
Pyrroloquinoline quinone (PQQ) is a naturally occurring redox-active compound with potent antioxidant, mitochondrial-enhancing, and neuroprotective properties. Originally identified as a cofactor in bacterial enzymes, PQQ has garnered significant interest for its potential therapeutic role in neurodegenerative diseases, including Alzheimer's disease (AD) and Parkinson's disease (PD). It has reported that PQQ exerts its effects through several key molecular mechanisms, including the activation of antioxidant pathways via Nrf2/ARE signaling, enhancement of mitochondrial biogenesis and function through AMPK/PGC-1α, and the regulation of inflammatory processes through NF-κB inhibition. By improving cellular energy metabolism, reducing oxidative stress, and promoting neuronal survival, PQQ offers a multifaceted approach to counteracting the pathophysiological factors underlying neurodegeneration. Our review focusing on current study of PQQ on its enhancing neuroplasticity, and protecting neurons from damage induced by oxidative stress, mitochondrial dysfunction, and inflammation. Further we reviewed the significant signaling pathways that involved PQQ neuroprotective mechanisms, positioning it as a novel candidate for future therapeutic strategies targeting these debilitating conditions.
吡咯喹啉醌(PQQ)是一种天然存在的具有氧化还原活性的化合物,具有强大的抗氧化、增强线粒体功能和神经保护特性。PQQ最初被鉴定为细菌酶中的一种辅因子,因其在包括阿尔茨海默病(AD)和帕金森病(PD)在内的神经退行性疾病中的潜在治疗作用而备受关注。据报道,PQQ通过几种关键的分子机制发挥作用,包括通过Nrf2/ARE信号通路激活抗氧化途径、通过AMPK/PGC-1α增强线粒体生物发生和功能,以及通过抑制NF-κB调节炎症过程。通过改善细胞能量代谢、减少氧化应激和促进神经元存活,PQQ提供了一种多方面的方法来对抗神经退行性变的病理生理因素。我们的综述聚焦于PQQ增强神经可塑性以及保护神经元免受氧化应激、线粒体功能障碍和炎症诱导损伤的当前研究。此外,我们还综述了涉及PQQ神经保护机制的重要信号通路,将其定位为未来针对这些衰弱性疾病的治疗策略的新候选物。