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Extracellular vesicles: multiple signaling capabilities and translation into promising therapeutic targets to promote neuronal plasticity. 细胞外囊泡:多种信号传导能力以及转化为促进神经元可塑性的有前途的治疗靶点。
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-12-01 Epub Date: 2024-11-13 DOI: 10.4103/NRR.NRR-D-24-00980
Dirk M Hermann, Bernd Giebel
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引用次数: 0
LPAR3: a shared target for neurodegenerative diseases? LPAR3:神经退行性疾病的共同靶点?
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-12-01 Epub Date: 2024-12-07 DOI: 10.4103/NRR.NRR-D-24-01024
Susan Acton, Laurent Chesnel
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引用次数: 0
A vascular endothelial growth factor-loaded chitosan-hyaluronic acid hydrogel scaffold enhances the therapeutic effect of adipose-derived stem cells in the context of stroke. 血管内皮生长因子负载壳聚糖透明质酸水凝胶支架增强了脂肪来源干细胞对中风的治疗效果。
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-12-01 Epub Date: 2024-09-06 DOI: 10.4103/NRR.NRR-D-24-00129
Zhijian Zheng, Xiaohui Lin, Zijun Zhao, Qiang Lin, Ji Liu, Manli Chen, Wenwen Wu, Zhiyun Wu, Nan Liu, Hongbin Chen

JOURNAL/nrgr/04.03/01300535-202512000-00028/figure1/v/2025-01-31T122243Z/r/image-tiff Adipose-derived stem cell, one type of mesenchymal stem cells, is a promising approach in treating ischemia-reperfusion injury caused by occlusion of the middle cerebral artery. However, its application has been limited by the complexities of the ischemic microenvironment. Hydrogel scaffolds, which are composed of hyaluronic acid and chitosan, exhibit excellent biocompatibility and biodegradability, making them promising candidates as cell carriers. Vascular endothelial growth factor is a crucial regulatory factor for stem cells. Both hyaluronic acid and chitosan have the potential to make the microenvironment more hospitable to transplanted stem cells, thereby enhancing the therapeutic effect of mesenchymal stem cell transplantation in the context of stroke. Here, we found that vascular endothelial growth factor significantly improved the activity and paracrine function of adipose-derived stem cells. Subsequently, we developed a chitosan-hyaluronic acid hydrogel scaffold that incorporated vascular endothelial growth factor and first injected the scaffold into an animal model of cerebral ischemia-reperfusion injury. When loaded with adipose-derived stem cells, this vascular endothelial growth factor-loaded scaffold markedly reduced neuronal apoptosis caused by oxygen-glucose deprivation/reoxygenation and substantially restored mitochondrial membrane potential and axon morphology. Further in vivo experiments revealed that this vascular endothelial growth factor-loaded hydrogel scaffold facilitated the transplantation of adipose-derived stem cells, leading to a reduction in infarct volume and neuronal apoptosis in a rat model of stroke induced by transient middle cerebral artery occlusion. It also helped maintain mitochondrial integrity and axonal morphology, greatly improving rat motor function and angiogenesis. Therefore, utilizing a hydrogel scaffold loaded with vascular endothelial growth factor as a stem cell delivery system can mitigate the adverse effects of ischemic microenvironment on transplanted stem cells and enhance the therapeutic effect of stem cells in the context of stroke.

脂肪来源干细胞是间充质干细胞的一种,是治疗大脑中动脉闭塞引起的缺血再灌注损伤的一种很有前景的方法。然而,缺血微环境的复杂性限制了它的应用。由透明质酸和壳聚糖组成的水凝胶支架具有良好的生物相容性和生物降解性,因此很有希望成为细胞载体。血管内皮生长因子是干细胞的重要调节因子。透明质酸和壳聚糖都有可能使微环境更有利于移植干细胞,从而增强间充质干细胞移植对中风的治疗效果。在这里,我们发现血管内皮生长因子能显著提高脂肪来源干细胞的活性和旁分泌功能。随后,我们开发了一种含有血管内皮生长因子的壳聚糖-透明质酸水凝胶支架,并首先将该支架注入脑缺血再灌注损伤动物模型。当负载脂肪来源干细胞时,这种负载血管内皮生长因子的支架明显减少了缺氧-葡萄糖/复氧引起的神经元凋亡,并大大恢复了线粒体膜电位和轴突形态。进一步的体内实验表明,这种负载血管内皮生长因子的水凝胶支架有助于移植脂肪来源的干细胞,从而在一过性大脑中动脉闭塞诱发的脑卒中大鼠模型中减少梗死体积和神经元凋亡。它还有助于维持线粒体完整性和轴突形态,大大改善了大鼠的运动功能和血管生成。因此,利用负载血管内皮生长因子的水凝胶支架作为干细胞输送系统,可以减轻缺血微环境对移植干细胞的不利影响,提高干细胞对中风的治疗效果。
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引用次数: 0
Alzheimer's disease and the immune system: the emerging role of TEMRA cells.
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-12-01 Epub Date: 2024-10-22 DOI: 10.4103/NRR.NRR-D-24-00793
Edric D Winford, Adam D Bachstetter
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引用次数: 0
Corrigendum: Neuroprotection by cattle encephalon glycoside and ignotin beyond the time window of thrombolysis in ischemic stroke. 更正:在缺血性中风溶栓时间窗之后,牛脑苷和点燃素对神经的保护作用。
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-12-01 Epub Date: 2025-01-31 DOI: 10.4103/NRR.NRR-D-24-01656
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引用次数: 0
Mitochondrial transplantation: a promising strategy for the treatment of retinal degenerative diseases.
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-12-01 Epub Date: 2024-12-07 DOI: 10.4103/NRR.NRR-D-24-00851
Jing Chi, Bin Fan, Yulin Li, Qing Jiao, Guang-Yu Li

The retina, a crucial neural tissue, is responsible for transforming light signals into visual information, a process that necessitates a significant amount of energy. Mitochondria, the primary powerhouses of the cell, play an integral role in retinal physiology by fulfilling the high-energy requirements of photoreceptors and secondary neurons through oxidative phosphorylation. In a healthy state, mitochondria ensure proper visual function by facilitating efficient conversion and transduction of visual signals. However, in retinal degenerative diseases, mitochondrial dysfunction significantly contributes to disease progression, involving a decline in membrane potential, the occurrence of DNA mutations, increased oxidative stress, and imbalances in quality-control mechanisms. These abnormalities lead to an inadequate energy supply, the exacerbation of oxidative damage, and the activation of cell death pathways, ultimately resulting in neuronal injury and dysfunction in the retina. Mitochondrial transplantation has emerged as a promising strategy for addressing these challenges. This procedure aims to restore metabolic activity and function in compromised cells through the introduction of healthy mitochondria, thereby enhancing the cellular energy production capacity and offering new strategies for the treatment of retinal degenerative diseases. Although mitochondrial transplantation presents operational and safety challenges that require further investigation, it has demonstrated potential for reviving the vitality of retinal neurons. This review offers a comprehensive examination of the principles and techniques underlying mitochondrial transplantation and its prospects for application in retinal degenerative diseases, while also delving into the associated technical and safety challenges, thereby providing references and insights for future research and treatment.

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引用次数: 0
Neuronal autosis: the self-destructive side of autophagy involved in hypoxic-ischemic neuronal death. 神经元自噬:自噬参与缺氧缺血性神经元死亡的自毁一面
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-12-01 Epub Date: 2024-11-13 DOI: 10.4103/NRR.NRR-D-24-00831
Vanessa Ginet, Pauline Depierre, Julien Puyal
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引用次数: 0
Systematic review of amyloid-beta clearance proteins from the brain to the periphery: implications for Alzheimer's disease diagnosis and therapeutic targets. 淀粉样蛋白- β清除蛋白从大脑到外周的系统综述:对阿尔茨海默病诊断和治疗靶点的影响
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-12-01 Epub Date: 2025-01-13 DOI: 10.4103/NRR.NRR-D-24-00865
Letian Huang, Mingyue Liu, Ze Li, Bing Li, Jiahe Wang, Ke Zhang

Amyloid-beta clearance plays a key role in the pathogenesis of Alzheimer's disease. However, the variation in functional proteins involved in amyloid-beta clearance and their correlation with amyloid-beta levels remain unclear. In this study, we conducted meta-analyses and a systematic review using studies from the PubMed, Embase, Web of Science, and Cochrane Library databases, including journal articles published from inception to June 30, 2023. The inclusion criteria included studies comparing the levels of functional proteins associated with amyloid-beta clearance in the blood, cerebrospinal fluid, and brain of healthy controls, patients with mild cognitive impairment, and patients with Alzheimer's disease. Additionally, we analyzed the correlation between these functional proteins and amyloid-beta levels in patients with Alzheimer's disease. The methodological quality of the studies was assessed via the Newcastle‒Ottawa Scale. Owing to heterogeneity, we utilized either a fixed-effect or random-effect model to assess the 95% confidence interval (CI) of the standard mean difference (SMD) among healthy controls, patients with mild cognitive impairment, and patients with Alzheimer's disease. The findings revealed significant alterations in the levels of insulin-degrading enzymes, neprilysin, matrix metalloproteinase-9, cathepsin D, receptor for advanced glycation end products, and P-glycoprotein in the brains of patients with Alzheimer's disease, patients with mild cognitive impairment, and healthy controls. In cerebrospinal fluid, the levels of triggering receptor expressed on myeloid cells 2 and ubiquitin C-terminal hydrolase L1 are altered, whereas the levels of TREM2, CD40, CD40L, CD14, CD22, cathepsin D, cystatin C, and α2 M in peripheral blood differ. Notably, TREM2 and cathepsin D showed changes in both brain (SMD = 0.31, 95% CI: 0.16-0.47, P < 0.001, I2 = 78.4%; SMD = 1.24, 95% CI: 0.01-2.48, P = 0.048, I2 = 90.1%) and peripheral blood (SMD = 1.01, 95% CI: 0.35-1.66, P = 0.003, I2 = 96.5%; SMD = 7.55, 95% CI: 3.92-11.18, P < 0.001, I2 = 98.2%) samples. Furthermore, correlations were observed between amyloid-beta levels and the levels of TREM2 ( r = 0.16, 95% CI: 0.04-0.28, P = 0.009, I2 = 74.7%), neprilysin ( r = -0.47, 95% CI: -0.80-0.14, P = 0.005, I2 = 76.1%), and P-glycoprotein ( r = -0.31, 95% CI: -0.51-0.11, P = 0.002, I2 = 0.0%) in patients with Alzheimer's disease. These findings suggest that triggering receptor expressed on myeloid cells 2 and cathepsin D could serve as potential diagnostic biomarkers for Alzheimer's disease, whereas triggering receptor expressed on myeloid cells 2, neprilysin, and P-glycoprotein may represent potential therapeutic targets.

淀粉样蛋白- β清除在阿尔茨海默病的发病机制中起着关键作用。然而,参与淀粉样蛋白- β清除的功能蛋白的变化及其与淀粉样蛋白- β水平的相关性尚不清楚。在这项研究中,我们对PubMed、Embase、Web of Science和Cochrane图书馆数据库的研究进行了荟萃分析和系统评价,包括从成立到2023年6月30日发表的期刊文章。纳入标准包括比较健康对照、轻度认知障碍患者和阿尔茨海默病患者血液、脑脊液和大脑中与淀粉样蛋白清除相关的功能蛋白水平的研究。此外,我们分析了这些功能蛋白与阿尔茨海默病患者β淀粉样蛋白水平之间的相关性。研究的方法学质量通过纽卡斯尔-渥太华量表进行评估。由于异质性,我们使用固定效应或随机效应模型来评估健康对照组、轻度认知障碍患者和阿尔茨海默病患者的标准平均差(SMD)的95%置信区间(CI)。研究结果显示,在阿尔茨海默病患者、轻度认知障碍患者和健康对照者的大脑中,胰岛素降解酶、neprilysin、基质金属蛋白酶-9、组织蛋白酶D、晚期糖基化终产物受体和p -糖蛋白的水平发生了显著变化。在脑脊液中,髓细胞2和泛素C末端水解酶L1的触发受体表达水平发生改变,而外周血TREM2、CD40、CD40L、CD14、CD22、组织蛋白酶D、胱抑素C和α2 M的表达水平不同。值得注意的是,TREM2和组织蛋白酶D在两脑均有变化(SMD = 0.31, 95% CI: 0.16-0.47, P < 0.001, I2 = 78.4%;SMD = 1.24, 95% CI: 0.01 ~ 2.48, P = 0.048, I2 = 90.1%)和外周血(SMD = 1.01, 95% CI: 0.35 ~ 1.66, P = 0.003, I2 = 96.5%;SMD = 7.55, 95% CI: 3.92 ~ 11.18, P < 0.001, I2 = 98.2%)样本。此外,在阿尔茨海默病患者中,淀粉样蛋白- β水平与TREM2 (r = 0.16, 95% CI: 0.04-0.28, P = 0.009, I2 = 74.7%)、neprilysin (r = -0.47, 95% CI: -0.80-0.14, P = 0.005, I2 = 76.1%)和P-糖蛋白(r = -0.31, 95% CI: -0.51-0.11, P = 0.002, I2 = 0.0%)水平存在相关性。这些发现表明,髓样细胞2和组织蛋白酶D上表达的触发受体可能作为阿尔茨海默病的潜在诊断生物标志物,而髓样细胞2、neprilysin和p -糖蛋白上表达的触发受体可能代表潜在的治疗靶点。
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引用次数: 0
Shedding light on the retina to see healthy and pathological aging. 照亮视网膜,看清健康和病理衰老。
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-12-01 Epub Date: 2024-10-22 DOI: 10.4103/NRR.NRR-D-24-00809
Marília Inês Móvio, Maria Camila Almeida, Sergio T Ferreira, Alexandre Hiroaki Kihara
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引用次数: 0
Nerve root magnetic stimulation regulates the synaptic plasticity of injured spinal cord by ascending sensory pathway.
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-12-01 Epub Date: 2025-01-13 DOI: 10.4103/NRR.NRR-D-24-00628
Ya Zheng, Lingyun Cao, Dan Zhao, Qi Yang, Chunya Gu, Yeran Mao, Guangyue Zhu, Yulian Zhu, Jing Zhao, Dongsheng Xu

JOURNAL/nrgr/04.03/01300535-202512000-00026/figure1/v/2025-01-31T122243Z/r/image-tiff Promoting synaptic plasticity and inducing functional reorganization of residual nerve fibers hold clinical significance for restoring motor function following spinal cord injury. Neuromagnetic stimulation targeting the nerve roots has been shown to improve motor function by enhancing nerve conduction in the injured spinal cord and restoring the synaptic ultrastructure of both the sensory and motor cortex. However, our understanding of the neurophysiological mechanisms by which nerve root magnetic stimulation facilitates motor function recovery in the spinal cord is limited, and its role in neuroplasticity remains unclear. In this study, we established a model of spinal cord injury in adult male Sprague-Dawley rats by applying moderate compression at the T10 vertebra. We then performed magnetic stimulation on the L5 nerve root for 3 weeks, beginning on day 3 post-injury. At day 22 post-injury, we observed that nerve root magnetic stimulation downregulated the level of interleukin-6 in the injured spinal cord tissue of rats. Additionally, this treatment reduced neuronal damage and glial scar formation, and increased the number of neurons in the injured spinal cord. Furthermore, nerve root magnetic stimulation decreased the levels of acetylcholine, norepinephrine, and dopamine, and increased the expression of synaptic plasticity-related mRNA and proteins PSD95, GAP43, and Synapsin II. Taken together, these results showed that nerve root magnetic stimulation alleviated neuronal damage in the injured spinal cord, regulated synaptic plasticity, and suppressed inflammatory responses. These findings provide laboratory evidence for the clinical application of nerve root magnetic stimulation in the treatment of spinal cord injury.

{"title":"Nerve root magnetic stimulation regulates the synaptic plasticity of injured spinal cord by ascending sensory pathway.","authors":"Ya Zheng, Lingyun Cao, Dan Zhao, Qi Yang, Chunya Gu, Yeran Mao, Guangyue Zhu, Yulian Zhu, Jing Zhao, Dongsheng Xu","doi":"10.4103/NRR.NRR-D-24-00628","DOIUrl":"https://doi.org/10.4103/NRR.NRR-D-24-00628","url":null,"abstract":"<p><p>JOURNAL/nrgr/04.03/01300535-202512000-00026/figure1/v/2025-01-31T122243Z/r/image-tiff Promoting synaptic plasticity and inducing functional reorganization of residual nerve fibers hold clinical significance for restoring motor function following spinal cord injury. Neuromagnetic stimulation targeting the nerve roots has been shown to improve motor function by enhancing nerve conduction in the injured spinal cord and restoring the synaptic ultrastructure of both the sensory and motor cortex. However, our understanding of the neurophysiological mechanisms by which nerve root magnetic stimulation facilitates motor function recovery in the spinal cord is limited, and its role in neuroplasticity remains unclear. In this study, we established a model of spinal cord injury in adult male Sprague-Dawley rats by applying moderate compression at the T10 vertebra. We then performed magnetic stimulation on the L5 nerve root for 3 weeks, beginning on day 3 post-injury. At day 22 post-injury, we observed that nerve root magnetic stimulation downregulated the level of interleukin-6 in the injured spinal cord tissue of rats. Additionally, this treatment reduced neuronal damage and glial scar formation, and increased the number of neurons in the injured spinal cord. Furthermore, nerve root magnetic stimulation decreased the levels of acetylcholine, norepinephrine, and dopamine, and increased the expression of synaptic plasticity-related mRNA and proteins PSD95, GAP43, and Synapsin II. Taken together, these results showed that nerve root magnetic stimulation alleviated neuronal damage in the injured spinal cord, regulated synaptic plasticity, and suppressed inflammatory responses. These findings provide laboratory evidence for the clinical application of nerve root magnetic stimulation in the treatment of spinal cord injury.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":"20 12","pages":"3564-3573"},"PeriodicalIF":5.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143648185","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
期刊
Neural Regeneration Research
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