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一氧化氮合酶中炎症介质调节的进展:对疾病调节和治疗方法的影响。

Advances in the Regulation of Inflammatory Mediators in Nitric Oxide Synthase: Implications for Disease Modulation and Therapeutic Approaches.

作者信息

Kim Mi Eun, Lee Jun Sik

机构信息

Immunology Research Lab, BK21-Four Educational Research Group for Age-associated Disorder Control Technology, Department of Biological Science, Chosun University, Gwangju 61452, Republic of Korea.

出版信息

Int J Mol Sci. 2025 Jan 30;26(3):1204. doi: 10.3390/ijms26031204.

DOI:10.3390/ijms26031204
PMID:39940974
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11818275/
Abstract

Nitric oxide synthases (NOS) are crucial enzymes responsible for the production of nitric oxide (NO), a signaling molecule with essential roles in vascular regulation, immune defense, and neurotransmission. The three NOS isoforms, endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS (iNOS), are tightly regulated by inflammatory mediators and cellular signaling pathways. While physiological NO production is vital for maintaining homeostasis, dysregulated NOS activity contributes to the pathogenesis of numerous diseases, including cardiovascular disorders, neurodegenerative conditions, and cancer. Recent advances in understanding the molecular mechanisms of NOS regulation have unveiled novel therapeutic opportunities, including isoform-specific modulators, upstream pathways, and nanotechnology-enhanced delivery systems. This review highlights these advancements, offering insights into how targeting NOS and its regulatory network can enable precise and effective therapeutic strategies for managing inflammation-driven pathologies.

摘要

一氧化氮合酶(NOS)是负责生成一氧化氮(NO)的关键酶,NO是一种信号分子,在血管调节、免疫防御和神经传递中发挥着重要作用。三种NOS同工型,即内皮型NOS(eNOS)、神经元型NOS(nNOS)和诱导型NOS(iNOS),受到炎症介质和细胞信号通路的严格调控。虽然生理性NO生成对于维持体内平衡至关重要,但NOS活性失调会导致多种疾病的发病机制,包括心血管疾病、神经退行性疾病和癌症。在理解NOS调节分子机制方面的最新进展揭示了新的治疗机会,包括同工型特异性调节剂、上游途径和纳米技术增强的递送系统。本综述重点介绍了这些进展,深入探讨了靶向NOS及其调节网络如何能够实现精确有效的治疗策略,以管理炎症驱动的病理状况。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cce2/11818275/fbabe0c789b7/ijms-26-01204-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cce2/11818275/fbabe0c789b7/ijms-26-01204-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cce2/11818275/fbabe0c789b7/ijms-26-01204-g001.jpg

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