Sun Yuanyuan, Wu Dan, Hu Qingxun
Shanghai Engineering Research Center of Organ Repair, School of Medicine, Shanghai University, Shanghai, 200444, China.
Institute of Geriatrics (Shanghai University), Affiliated Nantong Hospital of Shanghai University (The Sixth People's Hospital of Nantong), School of Medicine, Shanghai University, Nantong, 226011, China.
Curr Med Chem. 2024 Feb 16. doi: 10.2174/0109298673275187231121054541.
The nicotinamide adenine dinucleotide phosphate (NADP+/NADPH) redox couple serves as a substrate or cofactor for many enzymes to maintain cellular redox homeostasis as well as to regulate biosynthetic metabolism. The deficiency or imbalance of NADP+/NADPH redox couple is strongly associated with cardiovascular-related pathologies. An imbalance in the NADP+/NADPH ratio can lead to either oxidative or reductive stress. Reductive stress complicates the cellular redox environment and provides new insights into the cellular redox state. Newly discovered biosynthetic enzymes and developed genetically encoded biosensors provide technical support for studying how cells maintain a compartmentalized NADP(H) pool. NADP(H) plays an important role in cardiovascular pathologies. However, whether NADP(H) is injurious or protective in these diseases is uncertain, as either deficiency or excess NADP(H) levels can lead to imbalances in cellular redox state and metabolic homeostasis, resulting in energy stress, redox stress, and ultimately disease state. Additional study of the replicative regulatory network of NADP(H) metabolism in different compartments, and the mechanisms by which NADP(H) regulates redox state and metabolism under normal and pathological conditions, will develop the targeted and novel therapies based on NADP(H) metabolism.
烟酰胺腺嘌呤二核苷酸磷酸（NADP⁺/NADPH）氧化还原对作为许多酶的底物或辅助因子，以维持细胞氧化还原稳态并调节生物合成代谢。NADP⁺/NADPH氧化还原对的缺乏或失衡与心血管相关疾病密切相关。NADP⁺/NADPH比例的失衡可导致氧化应激或还原应激。还原应激使细胞氧化还原环境复杂化，并为细胞氧化还原状态提供了新的见解。新发现的生物合成酶和开发的基因编码生物传感器为研究细胞如何维持分隔的NADP（H）池提供了技术支持。NADP（H）在心血管疾病中起重要作用。然而，NADP（H）在这些疾病中是有害还是具有保护作用尚不确定，因为NADP（H）水平的缺乏或过量都可导致细胞氧化还原状态和代谢稳态失衡，从而导致能量应激、氧化还原应激，并最终导致疾病状态。进一步研究不同区室中NADP（H）代谢的复制调节网络，以及NADP（H）在正常和病理条件下调节氧化还原状态和代谢的机制，将开发基于NADP（H）代谢的靶向性和新型疗法。
