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Apolipoprotein A-I binding protein-mediated neuroprotection in glaucomatous neuroinflammation and neurodegeneration. 载脂蛋白 A-I 结合蛋白在青光眼神经炎症和神经变性中介导的神经保护作用
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-05-01 Epub Date: 2024-06-26 DOI: 10.4103/NRR.NRR-D-24-00221
Sinwoo Hwang, Seunghwan Choi, Soo-Ho Choi, Keun-Young Kim, Yury I Miller, Won-Kyu Ju
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引用次数: 0
The burden of upper motor neuron involvement is correlated with the bilateral limb involvement interval in patients with amyotrophic lateral sclerosis: a retrospective observational study. 肌萎缩侧索硬化症患者上运动神经元受累负担与双侧肢体受累间隔相关:一项回顾性观察研究。
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-05-01 Epub Date: 2024-03-01 DOI: 10.4103/NRR.NRR-D-23-01359
Jieying Wu, Shan Ye, Xiangyi Liu, Yingsheng Xu, Dongsheng Fan

JOURNAL/nrgr/04.03/01300535-202505000-00032/figure1/v/2024-07-28T173839Z/r/image-tiff Amyotrophic lateral sclerosis is a rare neurodegenerative disease characterized by the involvement of both upper and lower motor neurons. Early bilateral limb involvement significantly affects patients' daily lives and may lead them to be confined to bed. However, the effect of upper and lower motor neuron impairment and other risk factors on bilateral limb involvement is unclear. To address this issue, we retrospectively collected data from 586 amyotrophic lateral sclerosis patients with limb onset diagnosed at Peking University Third Hospital between January 2020 and May 2022. A univariate analysis revealed no significant differences in the time intervals of spread in different directions between individuals with upper motor neuron-dominant amyotrophic lateral sclerosis and those with classic amyotrophic lateral sclerosis. We used causal directed acyclic graphs for risk factor determination and Cox proportional hazards models to investigate the association between the duration of bilateral limb involvement and clinical baseline characteristics in amyotrophic lateral sclerosis patients. Multiple factor analyses revealed that higher upper motor neuron scores (hazard ratio [HR] = 1.05, 95% confidence interval [CI] = 1.01-1.09, P = 0.018), onset in the left limb (HR = 0.72, 95% CI = 0.58-0.89, P = 0.002), and a horizontal pattern of progression (HR = 0.46, 95% CI = 0.37-0.58, P < 0.001) were risk factors for a shorter interval until bilateral limb involvement. The results demonstrated that a greater degree of upper motor neuron involvement might cause contralateral limb involvement to progress more quickly in limb-onset amyotrophic lateral sclerosis patients. These findings may improve the management of amyotrophic lateral sclerosis patients with limb onset and the prediction of patient prognosis.

JOURNAL/nrgr/04.03/01300535-202505000-00032/figure1/v/2024-07-28T173839Z/r/image-tiff 肌萎缩侧索硬化症是一种罕见的神经退行性疾病,其特点是上下运动神经元均受累。早期的双侧肢体受累严重影响患者的日常生活,可能导致患者卧床不起。然而,上下运动神经元受损和其他风险因素对双侧肢体受累的影响尚不清楚。为了解决这个问题,我们回顾性地收集了2020年1月至2022年5月期间在北京大学第三医院确诊的586名肢体发病的肌萎缩侧索硬化症患者的数据。单变量分析显示,上运动神经元优势肌萎缩侧索硬化症患者与典型肌萎缩侧索硬化症患者在不同方向的扩散时间间隔上无显著差异。我们使用因果有向无环图确定风险因素,并使用 Cox 比例危险模型研究肌萎缩侧索硬化症患者双侧肢体受累持续时间与临床基线特征之间的关联。多因素分析表明,较高的上运动神经元评分(危险比 [HR] = 1.05,95% 置信区间 [CI] = 1.01-1.09,P = 0.018)、左侧肢体发病(HR = 0.72,95% CI = 0.58-0.89,P = 0.002)和水平进展模式(HR = 0.46,95% CI = 0.37-0.58,P < 0.001)是双侧肢体受累时间间隔较短的危险因素。研究结果表明,上运动神经元受累程度越高,肢端肌萎缩侧索硬化症患者的对侧肢体受累进展越快。这些发现可能会改善对肢体发病肌萎缩侧索硬化症患者的管理和对患者预后的预测。
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引用次数: 0
Translational machinery and translation regulation in axon regeneration. 轴突再生中的翻译机制和翻译调控
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-05-01 Epub Date: 2024-07-10 DOI: 10.4103/NRR.NRR-D-24-00313
Homaira Nawabi, Stephane Belin
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引用次数: 0
NECAB family of neuronal calcium-binding proteins in health and disease. 健康和疾病中的神经元钙结合蛋白 NECAB 家族。
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-05-01 Epub Date: 2024-06-26 DOI: 10.4103/NRR.NRR-D-24-00094
Diones Bueno, Michael K E Schäfer, Sudena Wang, Michael J Schmeisser, Axel Methner

The N-terminal EF-hand calcium-binding proteins 1-3 (NECAB1-3) constitute a family of predominantly neuronal proteins characterized by the presence of at least one EF-hand calcium-binding domain and a functionally less well characterized C-terminal antibiotic biosynthesis monooxygenase domain. All three family members were initially discovered due to their interactions with other proteins. NECAB1 associates with synaptotagmin-1, a critical neuronal protein involved in membrane trafficking and synaptic vesicle exocytosis. NECAB2 interacts with predominantly striatal G-protein-coupled receptors, while NECAB3 partners with amyloid-β A4 precursor protein-binding family A members 2 and 3, key regulators of amyloid-β production. This demonstrates the capacity of the family for interactions with various classes of proteins. NECAB proteins exhibit distinct subcellular localizations: NECAB1 is found in the nucleus and cytosol, NECAB2 resides in endosomes and the plasma membrane, and NECAB3 is present in the endoplasmic reticulum and Golgi apparatus. The antibiotic biosynthesis monooxygenase domain, an evolutionarily ancient component, is akin to atypical heme oxygenases in prokaryotes but is not well-characterized in vertebrates. Prokaryotic antibiotic biosynthesis monooxygenase domains typically form dimers, suggesting that calcium-mediated conformational changes in NECAB proteins may induce antibiotic biosynthesis monooxygenase domain dimerization, potentially activating some enzymatic properties. However, the substrate for this enzymatic activity remains uncertain. Alternatively, calcium-mediated conformational changes might influence protein interactions or the subcellular localization of NECAB proteins by controlling the availability of protein-protein interaction domains situated between the EF hands and the antibiotic biosynthesis monooxygenase domain. This review summarizes what is known about genomic organization, tissue expression, intracellular localization, interaction partners, and the physiological and pathophysiological role of the NECAB family.

摘要:N末端EF-手钙结合蛋白1-3(NECAB1-3)构成了一个主要由神经元蛋白组成的家族,其特征是至少存在一个EF-手钙结合结构域和一个功能上不太明显的C末端抗生素生物合成单加氧酶结构域。这三个家族成员最初都是通过与其他蛋白质的相互作用而被发现的。NECAB1 与突触标记蛋白-1 相关联,突触标记蛋白-1 是一种关键的神经元蛋白,参与膜贩运和突触囊泡的外泌。NECAB2 主要与纹状体 G 蛋白偶联受体相互作用,而 NECAB3 则与淀粉样β-A4 前体蛋白结合家族 A 成员 2 和 3(β-淀粉样蛋白生成的关键调节因子)合作。这表明该家族有能力与各类蛋白质相互作用。NECAB 蛋白具有不同的亚细胞定位:NECAB1 存在于细胞核和细胞膜中,NECAB2 存在于内体和质膜中,NECAB3 存在于内质网和高尔基体中。抗生素生物合成单加氧酶结构域是一个进化古老的组成部分,类似于原核生物中的非典型血红素加氧酶,但在脊椎动物中还没有得到很好的描述。原核生物抗生素生物合成单加氧酶结构域通常形成二聚体,这表明钙介导的 NECAB 蛋白构象变化可能诱导抗生素生物合成单加氧酶结构域二聚化,从而可能激活某些酶的特性。不过,这种酶活性的底物仍不确定。另外,钙介导的构象变化可能通过控制位于 EF 手和抗生素生物合成单加氧酶结构域之间的蛋白质-蛋白质相互作用结构域的可用性,影响蛋白质相互作用或 NECAB 蛋白的亚细胞定位。本综述总结了有关 NECAB 家族的基因组组织、组织表达、细胞内定位、相互作用伙伴以及生理和病理生理学作用的已知信息。
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引用次数: 0
Chondroitinase ABC combined with Schwann cell transplantation enhances restoration of neural connection and functional recovery following acute and chronic spinal cord injury. 软骨素酶ABC与许旺细胞移植相结合,可增强急慢性脊髓损伤后的神经连接恢复和功能恢复。
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-05-01 Epub Date: 2024-06-03 DOI: 10.4103/NRR.NRR-D-23-01338
Wenrui Qu, Xiangbing Wu, Wei Wu, Ying Wang, Yan Sun, Lingxiao Deng, Melissa Walker, Chen Chen, Heqiao Dai, Qi Han, Ying Ding, Yongzhi Xia, George Smith, Rui Li, Nai-Kui Liu, Xiao-Ming Xu

JOURNAL/nrgr/04.03/01300535-202505000-00029/figure1/v/2024-07-28T173839Z/r/image-tiff Schwann cell transplantation is considered one of the most promising cell-based therapy to repair injured spinal cord due to its unique growth-promoting and myelin-forming properties. A the Food and Drug Administration-approved Phase I clinical trial has been conducted to evaluate the safety of transplanted human autologous Schwann cells to treat patients with spinal cord injury. A major challenge for Schwann cell transplantation is that grafted Schwann cells are confined within the lesion cavity, and they do not migrate into the host environment due to the inhibitory barrier formed by injury-induced glial scar, thus limiting axonal reentry into the host spinal cord. Here we introduce a combinatorial strategy by suppressing the inhibitory extracellular environment with injection of lentivirus-mediated transfection of chondroitinase ABC gene at the rostral and caudal borders of the lesion site and simultaneously leveraging the repair capacity of transplanted Schwann cells in adult rats following a mid-thoracic contusive spinal cord injury. We report that when the glial scar was degraded by chondroitinase ABC at the rostral and caudal lesion borders, Schwann cells migrated for considerable distances in both rostral and caudal directions. Such Schwann cell migration led to enhanced axonal regrowth, including the serotonergic and dopaminergic axons originating from supraspinal regions, and promoted recovery of locomotor and urinary bladder functions. Importantly, the Schwann cell survival and axonal regrowth persisted up to 6 months after the injury, even when treatment was delayed for 3 months to mimic chronic spinal cord injury. These findings collectively show promising evidence for a combinatorial strategy with chondroitinase ABC and Schwann cells in promoting remodeling and recovery of function following spinal cord injury.

JOURNAL/nrgr/04.03/01300535-202505000-00029/figure1/v/2024-07-28T173839Z/r/image-tiff许旺细胞移植因其独特的促进生长和髓鞘形成特性,被认为是修复损伤脊髓最有前景的细胞疗法之一。美国食品和药物管理局批准了一项 I 期临床试验,以评估移植人类自体许旺细胞治疗脊髓损伤患者的安全性。许旺细胞移植面临的一个主要挑战是,移植的许旺细胞被限制在病变腔内,由于损伤引起的胶质瘢痕形成的抑制屏障,它们不会迁移到宿主环境中,从而限制了轴突重新进入宿主脊髓。在这里,我们引入了一种组合策略,通过在病变部位的喙侧和尾侧边界注射慢病毒介导的转染软骨素酶 ABC 基因来抑制细胞外的抑制性环境,同时利用移植的许旺细胞的修复能力来治疗成年大鼠中胸挫裂伤脊髓损伤。我们报告说,当软骨素酶 ABC 降解病变喙侧和尾侧边界的神经胶质瘢痕时,许旺细胞向喙侧和尾侧方向迁移了相当长的距离。这种许旺细胞迁移增强了轴突再生,包括源自脊髓上区的5-羟色胺能和多巴胺能轴突,并促进了运动和膀胱功能的恢复。重要的是,即使延迟治疗3个月以模拟慢性脊髓损伤,许旺细胞的存活和轴突再生在损伤后6个月仍能持续。这些研究结果共同表明,软骨素酶ABC和许旺细胞的组合策略在促进脊髓损伤后的重塑和功能恢复方面大有可为。
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引用次数: 0
The role of axon guidance molecules in the pathogenesis of epilepsy. 轴突导向分子在癫痫发病机制中的作用。
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-05-01 Epub Date: 2024-04-16 DOI: 10.4103/NRR.NRR-D-23-01620
Zheng Liu, Chunhua Pan, Hao Huang

Current treatments for epilepsy can only manage the symptoms of the condition but cannot alter the initial onset or halt the progression of the disease. Consequently, it is crucial to identify drugs that can target novel cellular and molecular mechanisms and mechanisms of action. Increasing evidence suggests that axon guidance molecules play a role in the structural and functional modifications of neural networks and that the dysregulation of these molecules is associated with epilepsy susceptibility. In this review, we discuss the essential role of axon guidance molecules in neuronal activity in patients with epilepsy as well as the impact of these molecules on synaptic plasticity and brain tissue remodeling. Furthermore, we examine the relationship between axon guidance molecules and neuroinflammation, as well as the structural changes in specific brain regions that contribute to the development of epilepsy. Ample evidence indicates that axon guidance molecules, including semaphorins and ephrins, play a fundamental role in guiding axon growth and the establishment of synaptic connections. Deviations in their expression or function can disrupt neuronal connections, ultimately leading to epileptic seizures. The remodeling of neural networks is a significant characteristic of epilepsy, with axon guidance molecules playing a role in the dynamic reorganization of neural circuits. This, in turn, affects synapse formation and elimination. Dysregulation of these molecules can upset the delicate balance between excitation and inhibition within a neural network, thereby increasing the risk of overexcitation and the development of epilepsy. Inflammatory signals can regulate the expression and function of axon guidance molecules, thus influencing axonal growth, axon orientation, and synaptic plasticity. The dysregulation of neuroinflammation can intensify neuronal dysfunction and contribute to the occurrence of epilepsy. This review delves into the mechanisms associated with the pathogenicity of axon guidance molecules in epilepsy, offering a valuable reference for the exploration of therapeutic targets and presenting a fresh perspective on treatment strategies for this condition.

目前治疗癫痫的方法只能控制病情的症状,但无法改变最初的发病或阻止病情的发展。因此,找出能够针对新型细胞和分子机制及作用机制的药物至关重要。越来越多的证据表明,轴突导向分子在神经网络的结构和功能改变中发挥作用,而这些分子的失调与癫痫易感性有关。在这篇综述中,我们将讨论轴突导向分子在癫痫患者神经元活动中的重要作用,以及这些分子对突触可塑性和脑组织重塑的影响。此外,我们还研究了轴突导向分子与神经炎症之间的关系,以及导致癫痫发生的特定脑区结构变化。大量证据表明,轴突导向分子(包括semaphorins和ephrins)在引导轴突生长和建立突触连接方面发挥着重要作用。它们的表达或功能偏差会破坏神经元连接,最终导致癫痫发作。神经网络的重塑是癫痫的一个重要特征,轴突导向分子在神经回路的动态重组中发挥着作用。这反过来又会影响突触的形成和消除。这些分子的失调会破坏神经网络内兴奋和抑制之间的微妙平衡,从而增加过度兴奋和发展成癫痫的风险。炎症信号可调节轴突导向分子的表达和功能,从而影响轴突生长、轴突定向和突触可塑性。神经炎症的失调会加剧神经元功能障碍,导致癫痫的发生。这篇综述深入探讨了轴突导向分子在癫痫中的致病机制,为探索治疗靶点提供了宝贵的参考,并为该疾病的治疗策略提供了全新的视角。
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引用次数: 0
Combinatorial therapies for spinal cord injury repair. 脊髓损伤修复的组合疗法。
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-05-01 Epub Date: 2024-06-03 DOI: 10.4103/NRR.NRR-D-24-00061
Carla S Sousa, Andreia Monteiro, António J Salgado, Nuno A Silva

Spinal cord injuries have profound detrimental effects on individuals, regardless of whether they are caused by trauma or non-traumatic events. The compromised regeneration of the spinal cord is primarily attributed to damaged neurons, inhibitory molecules, dysfunctional immune response, and glial scarring. Unfortunately, currently, there are no effective treatments available that can fully repair the spinal cord and improve functional outcomes. Nevertheless, numerous pre-clinical approaches have been studied for spinal cord injury recovery, including using biomaterials, cells, drugs, or technological-based strategies. Combinatorial treatments, which target various aspects of spinal cord injury pathophysiology, have been extensively tested in the last decade. These approaches aim to synergistically enhance repair processes by addressing various obstacles faced during spinal cord regeneration. Thus, this review intends to provide scientists and clinicians with an overview of pre-clinical combinatorial approaches that have been developed toward the solution of spinal cord regeneration as well as update the current knowledge about spinal cord injury pathophysiology with an emphasis on the current clinical management.

摘要:无论脊髓损伤是由外伤还是非外伤造成的,都会对个人产生深远的不利影响。脊髓再生功能受损的主要原因是神经元受损、抑制分子、免疫反应失调和神经胶质瘢痕。遗憾的是,目前还没有有效的治疗方法可以完全修复脊髓并改善功能结果。尽管如此,临床前已研究出许多脊髓损伤恢复方法,包括使用生物材料、细胞、药物或基于技术的策略。在过去十年中,针对脊髓损伤病理生理学各个方面的组合疗法已得到广泛测试。这些方法旨在通过解决脊髓再生过程中面临的各种障碍,协同增强修复过程。因此,本综述旨在向科学家和临床医生概述为解决脊髓再生问题而开发的临床前组合疗法,并更新当前有关脊髓损伤病理生理学的知识,重点介绍当前的临床治疗方法。
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引用次数: 0
Pharmacological intervention for chronic phase of spinal cord injury. 对脊髓损伤慢性期进行药物干预。
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-05-01 Epub Date: 2024-06-26 DOI: 10.4103/NRR.NRR-D-24-00176
Chihiro Tohda

Spinal cord injury is an intractable traumatic injury. The most common hurdles faced during spinal cord injury are failure of axonal regrowth and reconnection to target sites. These also tend to be the most challenging issues in spinal cord injury. As spinal cord injury progresses to the chronic phase, lost motor and sensory functions are not recovered. Several reasons may be attributed to the failure of recovery from chronic spinal cord injury. These include factors that inhibit axonal growth such as activated astrocytes, chondroitin sulfate proteoglycan, myelin-associated proteins, inflammatory microglia, and fibroblasts that accumulate at lesion sites. Skeletal muscle atrophy due to denervation is another chronic and detrimental spinal cord injury-specific condition. Although several intervention strategies based on multiple outlooks have been attempted for treating spinal cord injury, few approaches have been successful. To treat chronic spinal cord injury, neural cells or tissue substitutes may need to be supplied in the cavity area to enable possible axonal growth. Additionally, stimulating axonal growth activity by extrinsic factors is extremely important and essential for maintaining the remaining host neurons and transplanted neurons. This review focuses on pharmacotherapeutic approaches using small compounds and proteins to enable axonal growth in chronic spinal cord injury. This review presents some of these candidates that have shown promising outcomes in basic research ( in vivo animal studies) and clinical trials: AA-NgR(310)ecto-Fc (AXER-204), fasudil, phosphatase and tensin homolog protein antagonist peptide 4, chondroitinase ABC, intracellular sigma peptide, (-)-epigallocatechin gallate, matrine, acteoside, pyrvate kinase M2, diosgenin, granulocyte-colony stimulating factor, and fampridine-sustained release. Although the current situation suggests that drug-based therapies to recover function in chronic spinal cord injury are limited, potential candidates have been identified through basic research, and these candidates may be subjects of clinical studies in the future. Moreover, cocktail therapy comprising drugs with varied underlying mechanisms may be effective in treating the refractory status of chronic spinal cord injury.

摘要:脊髓损伤是一种难治性创伤。脊髓损伤期间最常见的障碍是轴突再生失败和目标部位的重新连接。这些也往往是脊髓损伤中最具挑战性的问题。随着脊髓损伤发展到慢性阶段,失去的运动和感觉功能无法恢复。慢性脊髓损伤无法恢复可能有几个原因。其中包括抑制轴突生长的因素,如激活的星形胶质细胞、硫酸软骨素蛋白多糖、髓鞘相关蛋白、炎症性小胶质细胞以及聚集在病变部位的成纤维细胞。神经支配导致的骨骼肌萎缩是脊髓损伤特有的另一种慢性有害症状。尽管基于多种观点的干预策略已被尝试用于治疗脊髓损伤,但成功的方法却寥寥无几。要治疗慢性脊髓损伤,可能需要在空腔区域提供神经细胞或组织替代物,以使轴突生长成为可能。此外,通过外在因子刺激轴突生长活性对于维持剩余的宿主神经元和移植神经元极为重要,也是必不可少的。本综述重点介绍利用小分子化合物和蛋白质促进慢性脊髓损伤患者轴突生长的药物治疗方法。本综述介绍了其中一些在基础研究(体内动物研究)和临床试验中显示出良好效果的候选药物:AA-NgR(310)ecto-Fc(AXER-204)、法舒地尔、磷酸酶和天丝同源蛋白(PTEN)拮抗剂肽4、软骨素酶ABC、细胞内σ肽、(-)-表没食子儿茶素没食子酸酯、马替林、肌动蛋白苷、吡咯烷酮激酶M2、薯蓣皂苷、粒细胞集落刺激因子和泛影葡胺持续释放。虽然从目前的情况来看,恢复慢性脊髓损伤功能的药物疗法还很有限,但通过基础研究已经发现了潜在的候选药物,这些候选药物将来可能会成为临床研究的对象。此外,由具有不同基本机制的药物组成的鸡尾酒疗法可能对治疗慢性脊髓损伤的难治性状态有效。
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引用次数: 0
Exercise preconditioning alleviates ischemia-induced memory deficits by increasing circulating adiponectin. 运动预处理通过增加循环脂肪连接蛋白缓解缺血诱导的记忆缺陷
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-05-01 Epub Date: 2024-03-01 DOI: 10.4103/NRR.NRR-D-23-01101
Meifeng Zheng, Borui Zhang, Sonata S Y Yau, Kwok-Fai So, Li Zhang, Haining Ou

JOURNAL/nrgr/04.03/01300535-202505000-00027/figure1/v/2024-07-28T173839Z/r/image-tiff Cerebral ischemia is a major health risk that requires preventive approaches in addition to drug therapy. Physical exercise enhances neurogenesis and synaptogenesis, and has been widely used for functional rehabilitation after stroke. In this study, we determined whether exercise training before disease onset can alleviate the severity of cerebral ischemia. We also examined the role of exercise-induced circulating factors in these effects. Adult mice were subjected to 14 days of treadmill exercise training before surgery for middle cerebral artery occlusion. We found that this exercise pre-conditioning strategy effectively attenuated brain infarct area, inhibited gliogenesis, protected synaptic proteins, and improved novel object and spatial memory function. Further analysis showed that circulating adiponectin plays a critical role in these preventive effects of exercise. Agonist activation of adiponectin receptors by AdipoRon mimicked the effects of exercise, while inhibiting receptor activation abolished the exercise effects. In summary, our results suggest a crucial role of circulating adiponectin in the effects of exercise pre-conditioning in protecting against cerebral ischemia and supporting the health benefits of exercise.

JOURNAL/nrgr/04.03/01300535-202505000-00027/figure1/v/2024-07-28T173839Z/r/image-tiff脑缺血是一种主要的健康风险,除了药物治疗外,还需要采取预防方法。体育锻炼可促进神经发生和突触生成,已被广泛用于脑卒中后的功能康复。在本研究中,我们确定了发病前的运动训练是否能减轻脑缺血的严重程度。我们还研究了运动诱导的循环因子在这些效应中的作用。成年小鼠在大脑中动脉闭塞手术前接受了为期 14 天的跑步机运动训练。我们发现,这种运动预处理策略能有效减小脑梗塞面积、抑制胶质生成、保护突触蛋白,并改善新物体和空间记忆功能。进一步的分析表明,循环中的脂肪连接蛋白在运动的这些预防作用中发挥了关键作用。AdipoRon 对脂肪连接素受体的激动剂激活模拟了运动的效果,而抑制受体激活则消除了运动的效果。总之,我们的研究结果表明,循环中的脂肪连接蛋白在运动预处理保护脑缺血和支持运动对健康的益处方面起着至关重要的作用。
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引用次数: 0
Lactate is a potentially harmful substitute for brain glucose fuel: consequences for metabolic restoration of neurotransmission. 乳酸盐是脑葡萄糖燃料的潜在有害替代品:对神经传递的代谢恢复的影响。
IF 5.9 2区 医学 Q2 CELL BIOLOGY Pub Date : 2025-05-01 Epub Date: 2024-06-03 DOI: 10.4103/NRR.NRR-D-24-00262
Oliver Kann, Lennart Söder, Babak Khodaie
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引用次数: 0
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