Exosome-mediated miRNA delivery: a molecular switch for reshaping neuropathic pain therapy.

IF 3.8 3区 医学 Q2 NEUROSCIENCES
Frontiers in Molecular Neuroscience Pub Date : 2025-07-04 eCollection Date: 2025-01-01 DOI:10.3389/fnmol.2025.1625943
Ziqing Wei, Chunhui Guo, Hang Zhou, Yanling Wu, Xudong Zhou, Jibing Chen, Fujun Li
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引用次数: 0

Abstract

Neuropathic pain (NP) is a chronic condition caused by nerve injury or disease. It remains a therapeutic challenge because conventional drugs have limited efficacy and cause adverse effects. Exosomes, with the ability to cross the blood-brain barrier, low immunogenicity, and tissue-homing capacity, have emerged as promising nanovehicles for precise microRNA (miRNA) delivery to modulate key NP pathologies such as neuroinflammation, neuronal hyperexcitability, mechanical allodynia, and thermal hyperalgesia. In this review, we highlight recent advances in exosome-mediated miRNA therapy for NP. We also elucidate the molecular mechanisms and unique advantages of exosomes as both delivery platforms and intrinsic therapeutic agents. We synthesize evidence from preclinical models and initial clinical-stage studies, addressing translational challenges in scalable production and targeted delivery. Through sustained innovation and multidisciplinary collaboration, exosome-based miRNA delivery systems demonstrate transformative potential to overcome current therapeutic limitations, enabling novel NP management strategies.

外泌体介导的miRNA传递:重塑神经性疼痛治疗的分子开关。
神经性疼痛是一种由神经损伤或疾病引起的慢性疾病。这仍然是一个治疗上的挑战,因为传统药物的疗效有限,而且会造成不良反应。外泌体具有穿越血脑屏障的能力、低免疫原性和组织归巢能力,已成为有前途的纳米载体,用于精确递送microRNA (miRNA),以调节关键的NP病理,如神经炎症、神经元高兴奋性、机械异常性疼痛和热痛觉过敏。在这篇综述中,我们重点介绍了外泌体介导的miRNA治疗NP的最新进展。我们还阐明了外泌体作为递送平台和内在治疗剂的分子机制和独特优势。我们综合临床前模型和初步临床阶段研究的证据,解决可扩展生产和靶向交付的转化挑战。通过持续的创新和多学科合作,基于外泌体的miRNA传递系统展示了克服当前治疗限制的变革潜力,实现了新的NP管理策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
5.70
自引率
2.10%
发文量
669
审稿时长
14 weeks
期刊介绍: Frontiers in Molecular Neuroscience is a first-tier electronic journal devoted to identifying key molecules, as well as their functions and interactions, that underlie the structure, design and function of the brain across all levels. The scope of our journal encompasses synaptic and cellular proteins, coding and non-coding RNA, and molecular mechanisms regulating cellular and dendritic RNA translation. In recent years, a plethora of new cellular and synaptic players have been identified from reduced systems, such as neuronal cultures, but the relevance of these molecules in terms of cellular and synaptic function and plasticity in the living brain and its circuits has not been validated. The effects of spine growth and density observed using gene products identified from in vitro work are frequently not reproduced in vivo. Our journal is particularly interested in studies on genetically engineered model organisms (C. elegans, Drosophila, mouse), in which alterations in key molecules underlying cellular and synaptic function and plasticity produce defined anatomical, physiological and behavioral changes. In the mouse, genetic alterations limited to particular neural circuits (olfactory bulb, motor cortex, cortical layers, hippocampal subfields, cerebellum), preferably regulated in time and on demand, are of special interest, as they sidestep potential compensatory developmental effects.
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