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<p>Perioperative neurocognitive disorders (PND) are prevalent complications in elderly patients following surgery, characterized by cognitive decline and memory impairment. This study investigates the contribution of plasma-derived exosomal microRNA hsa-miR-3677-3p to PND pathogenesis via <i>ABCB8</i> regulation and subsequent induction of neuronal ferroptosis. Exosomes were isolated from plasma of patients with delayed neurocognitive recovery (dNCR) and non-dNCR patients. Characterization confirmed successful exosome isolation, revealing distinct microRNA profiles between the two groups. MicroRNA sequencing identified 69 differentially expressed microRNAs, with hsa-miR-3677-3p significantly upregulated in dNCR patients. Functional enrichment analysis implicated these microRNAs in mitochondrial function and nervous system development. In vitro overexpression of hsa-miR-3677-3p mimicked the pathological phenotype, leading to downregulation of ABCB8, which resulted in iron dyshomeostasis and oxidative stress, marked by reduced antioxidant capacity, intracellular iron accumulation, elevated malondialdehyde (MDA), a decreased glutathione/glutathione disulfide (GSH/GSSG) ratio, and increased mitochondrial lipid peroxidation (MitoPerOx). Treatment with the ferroptosis inhibitor Ferrostatin-1 (Fer-1) attenuated these alterations, restoring mitochondrial function and reducing oxidative damage. Taken together, our findings indicate that exosomal hsa-miR-3677-3p modulates <i>ABCB8</i>-mediated ferroptosis in neurons, highlighting a novel insight into PND pathogenesis and potential therapeutic strategies.</p>

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Plasma-Derived Exosomal hsa-miR-3677-3p Induces Ferroptosis in Neurons by Targeting ABCB8 in Perioperative Neurocognitive Disorders After Prostate Surgery

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月24日

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  • Yiyan Sun,
  • Yuanyuan Zuo,
  • Jingya Zhang,
  • Ying Wu,
  • Xiaohuan Xia,
  • Jianhui Liu

摘要

Perioperative neurocognitive disorders (PND) are prevalent complications in elderly patients following surgery, characterized by cognitive decline and memory impairment. This study investigates the contribution of plasma-derived exosomal microRNA hsa-miR-3677-3p to PND pathogenesis via ABCB8 regulation and subsequent induction of neuronal ferroptosis. Exosomes were isolated from plasma of patients with delayed neurocognitive recovery (dNCR) and non-dNCR patients. Characterization confirmed successful exosome isolation, revealing distinct microRNA profiles between the two groups. MicroRNA sequencing identified 69 differentially expressed microRNAs, with hsa-miR-3677-3p significantly upregulated in dNCR patients. Functional enrichment analysis implicated these microRNAs in mitochondrial function and nervous system development. In vitro overexpression of hsa-miR-3677-3p mimicked the pathological phenotype, leading to downregulation of ABCB8, which resulted in iron dyshomeostasis and oxidative stress, marked by reduced antioxidant capacity, intracellular iron accumulation, elevated malondialdehyde (MDA), a decreased glutathione/glutathione disulfide (GSH/GSSG) ratio, and increased mitochondrial lipid peroxidation (MitoPerOx). Treatment with the ferroptosis inhibitor Ferrostatin-1 (Fer-1) attenuated these alterations, restoring mitochondrial function and reducing oxidative damage. Taken together, our findings indicate that exosomal hsa-miR-3677-3p modulates ABCB8-mediated ferroptosis in neurons, highlighting a novel insight into PND pathogenesis and potential therapeutic strategies.