Neurochemistry international最新文献_第3页

CB1 receptor signaling: Linking neuroplasticity, neuronal types, and mental health outcomes

IF 4.4 3区医学

Neurochemistry international Pub Date : 2025-02-02 DOI: 10.1016/j.neuint.2025.105938

Qianqian Gao , Muhammad Asim

{"title":"CB1 receptor signaling: Linking neuroplasticity, neuronal types, and mental health outcomes","authors":"Qianqian Gao , Muhammad Asim","doi":"10.1016/j.neuint.2025.105938","DOIUrl":"10.1016/j.neuint.2025.105938","url":null,"abstract":"<div><div>The endocannabinoid system (ECS) is crucial in the pathophysiology of mental disorders. Historically, cannabis has been utilized for centuries to mitigate symptoms of anxiety and depression; however, the precise role of cannabinoids in these conditions has only recently garnered extensive research attention. Despite the growing body of literature on the ECS and its association with mental health, several critical questions remain unresolved. This review primarily focuses on cannabinoid CB<sub>1</sub> receptors (CB<sub>1</sub>R), providing an examination of their regulatory roles in states related to mental disorders. Evidence suggests that CB<sub>1</sub>R distribution occurs among various neuronal types, astrocytes, and subcellular membranes across multiple brain regions, potentially exhibiting both analogous and antagonistic effects. Additionally, various forms of stress have been shown to produce divergent impacts on CB<sub>1</sub>R signaling pathways. Furthermore, numerous CB<sub>1</sub>R agonists demonstrate biphasic, dose-dependent effects on anxiety and depression; specifically, low doses may exert anxiolytic effects, while higher doses can induce anxiogenic responses, a phenomenon observed in both rodent models and human studies. We also discuss the diverse underlying mechanisms that mediate these effects. We anticipate that this review will yield valuable insights into the role of CB<sub>1</sub>R in mental disorders and provide a framework for future research endeavors on CB<sub>1</sub>R and the ECS. This knowledge may ultimately inform therapeutic strategies aimed at alleviating symptoms associated with mental health conditions.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"184 ","pages":"Article 105938"},"PeriodicalIF":4.4,"publicationDate":"2025-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143187730","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Understanding the intricacies of cellular mechanisms in remyelination: The role of circadian rhythm 理解髓鞘再生中细胞机制的复杂性：昼夜节律的作用。

IF 4.4 3区医学

Neurochemistry international Pub Date : 2025-02-01 DOI: 10.1016/j.neuint.2025.105929

Yufen Tang , Lu Zhang , Peng Huang , Zhou She , Senlin Luo , Hong Peng , Yuqiong Chen , Jinwen Luo , Wangxin Duan , Yangyang Xiao , Lingjuan Liu , Liqun Liu

{"title":"Understanding the intricacies of cellular mechanisms in remyelination: The role of circadian rhythm","authors":"Yufen Tang , Lu Zhang , Peng Huang , Zhou She , Senlin Luo , Hong Peng , Yuqiong Chen , Jinwen Luo , Wangxin Duan , Yangyang Xiao , Lingjuan Liu , Liqun Liu","doi":"10.1016/j.neuint.2025.105929","DOIUrl":"10.1016/j.neuint.2025.105929","url":null,"abstract":"<div><div>The term “circadian rhythm” refers to the 24-h oscillations found in various physiological processes in organisms, responsible for maintaining bodily homeostasis. Many neurological diseases mainly involve the process of demyelination, and remyelination is crucial for the treatment of neurological diseases. Current research mainly focuses on the key role of circadian clocks in the pathophysiological mechanisms of multiple sclerosis. Various studies have shown that the circadian rhythm regulates various cellular molecular mechanisms and signaling pathways involved in remyelination. The process of remyelination is primarily mediated by oligodendrocyte precursor cells (OPCs), oligodendrocytes, microglia, and astrocytes. OPCs are activated, proliferate, migrate, and ultimately differentiate into oligodendrocytes after demyelination, involving many key signaling pathway and regulatory factors. Activated microglia secretes important cytokines and chemokines, promoting OPC proliferation and differentiation, and phagocytoses myelin debris that inhibits remyelination. Astrocytes play a crucial role in supporting remyelination by secreting signals that promote remyelination or facilitate the phagocytosis of myelin debris by microglia. Additionally, cell-to-cell communication via gap junctions allows for intimate contact between astrocytes and oligodendrocytes, providing metabolic support for oligodendrocytes. Therefore, gaining a deeper understanding of the mechanisms and molecular pathways of the circadian rhythm at various stages of remyelination can help elucidate the fundamental characteristics of remyelination and provide insights into treating demyelinating disorders.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"183 ","pages":"Article 105929"},"PeriodicalIF":4.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A topographic approach to the markers of macrophage/microglia and other cell types in high grade glioma 高级别胶质瘤中巨噬细胞/小胶质细胞和其他细胞类型标记物的地形学研究。

IF 4.4 3区医学

Neurochemistry international Pub Date : 2025-02-01 DOI: 10.1016/j.neuint.2024.105922

Lucia Lisi , Alessandro Olivi , Gabriella Maria Pia Ciotti , Salvatore Marino , Chiara Ferraro , Grazia Menna , Maria Martire , Giovanni Pennisi , Pierluigi Navarra , Giuseppe Maria della Pepa

{"title":"A topographic approach to the markers of macrophage/microglia and other cell types in high grade glioma","authors":"Lucia Lisi , Alessandro Olivi , Gabriella Maria Pia Ciotti , Salvatore Marino , Chiara Ferraro , Grazia Menna , Maria Martire , Giovanni Pennisi , Pierluigi Navarra , Giuseppe Maria della Pepa","doi":"10.1016/j.neuint.2024.105922","DOIUrl":"10.1016/j.neuint.2024.105922","url":null,"abstract":"<div><div>In glioblastoma, glioma-associated microglia/macrophages (GAMs) represent the major population of tumor infiltrating cells, with up to one half of the cells of the tumor mass. Recent studies have shown that microglia are involved in the maintenance of immunological homeostasis and protection against autoimmunity. However, despite the growing body of evidence on the topic, many aspects are yet to be clarified. In our study, 3 different situations emerged concerning the markers of microglial/macrophage-related and other cell types in GBM patients: i) most of the markers (IBA1, TMEM119, CD206 and CD86) show an ascending gradient from the tumor center to the non-tumor/healthy area of the brain; ii) one marker (CD204) shows a descending gradient, going from the center of the tumor to the non-tumor/healthy brain area; iii) two markers (CD163 and P2RY12) show no gradient. These observations support the idea that the magnitude of the diverted inflammation is a ‘extensive’ rather than a ‘local’ phenomenon and that could possibly play a role in disease resistance and relapse.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"183 ","pages":"Article 105922"},"PeriodicalIF":4.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142902487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Previous strength training attenuates ouabain-induced bipolar disorder-related behaviors and memory deficits in rats: Involvement of hippocampal ERK/CREB and PI3K/AKT/mTOR pathways 先前的力量训练减弱了大鼠的维卡因诱导的双相情感障碍相关行为和记忆缺陷：海马ERK/CREB和PI3K/AKT/mTOR通路的参与

IF 4.4 3区医学

Neurochemistry international Pub Date : 2025-02-01 DOI: 10.1016/j.neuint.2024.105919

Luan Machado Maidana , Jozyê Milena da Silva Guerra , Adson Souza-Pereira , Marizabel Parente Lins , Mayckel Jean Moreira-Silva , Eduarda Goulart Paiva , Douglas Buchmann Godinho , Luis Fernando Freire Royes , Leonardo Magno Rambo

{"title":"Previous strength training attenuates ouabain-induced bipolar disorder-related behaviors and memory deficits in rats: Involvement of hippocampal ERK/CREB and PI3K/AKT/mTOR pathways","authors":"Luan Machado Maidana , Jozyê Milena da Silva Guerra , Adson Souza-Pereira , Marizabel Parente Lins , Mayckel Jean Moreira-Silva , Eduarda Goulart Paiva , Douglas Buchmann Godinho , Luis Fernando Freire Royes , Leonardo Magno Rambo","doi":"10.1016/j.neuint.2024.105919","DOIUrl":"10.1016/j.neuint.2024.105919","url":null,"abstract":"<div><div>Bipolar disorder (BD) is a central nervous system condition that is typified by fluctuations in mood, oscillating between depressive and manic, and/or hypomanic episodes. The objective of this study was to test the hypothesis that strength training may act as a potent protector against behavioral and neurochemical changes induced by BD. A strength training protocol was performed with adult male Wistar rats, and seven days following the conclusion of training, a single ouabain injection was administered. Following ouabain administration, the animals were subjected to behavioral tests after the seventh (manic period) and fourteenth (depressive period) days. Subsequently, rats were euthanized and the hippocampus was collected for western blotting assays. We demonstrated that strength training provided protection against ouabain-induced behavioral changes, both during the manic and depressive periods, including increased locomotor activity, risk-taking and aggressive-like behaviors, and impaired memory performance. Furthermore, physical training protected against ouabain-induced decrease of neurogenesis/neuroplasticity-related pathways, including BDNF/TrKB/ERK/CREB and PI3K/AKT/mTOR/p70S6K. These findings suggest that strength training has a protective effect, attenuating or preventing BD-induced deficits, and may have therapeutic potential as an adjuvant treatment for this patient population in the future.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"183 ","pages":"Article 105919"},"PeriodicalIF":4.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142884937","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Celecoxib paradoxically induces COX-2 expression and astrocyte activation through the ERK/JNK/AP-1 signaling pathway in the cerebral cortex of rats 塞来昔布通过ERK/JNK/AP-1信号通路矛盾地诱导大鼠大脑皮层COX-2表达和星形胶质细胞活化。

IF 4.4 3区医学

Neurochemistry international Pub Date : 2025-02-01 DOI: 10.1016/j.neuint.2024.105926

Kai-Che Wei , Jun-Ting Lin , Chia-Ho Lin

{"title":"Celecoxib paradoxically induces COX-2 expression and astrocyte activation through the ERK/JNK/AP-1 signaling pathway in the cerebral cortex of rats","authors":"Kai-Che Wei , Jun-Ting Lin , Chia-Ho Lin","doi":"10.1016/j.neuint.2024.105926","DOIUrl":"10.1016/j.neuint.2024.105926","url":null,"abstract":"<div><div>Previous studies have shown that celecoxib or NSAID may paradoxically induce cyclooxygenase-2 (COX-2) expression and trigger inflammation-like responses in airway smooth muscle cells and renal mesangial cells. Despite the extensive research on celecoxib, its atypical biological effect on the induction of COX-2 in astroglial cells within the central nervous system (CNS) remains unexplored. In the present study, we investigated the impact of celecoxib on COX-2 and Glial Fibrillary Acidic Protein (GFAP) expression and explored the mechanisms underlying celecoxib-regulated COX-2 expression in cortical astrocytes of rats.</div><div>Cortical astrocytes were treated with celecoxib (20 μM) for 24 h, resulting in a significant increase in COX-2 expression and up-regulation of GFAP, a marker of astrocyte activation, and the COX-2 induced by celecoxib is functionally active in prostaglandin E2 (PGE2) synthesis. Celecoxib also enhanced LPS-induced COX-2 expression, but its ability to inhibit PGE2 synthesis decreased at higher concentrations. Celecoxib induced phosphorylation of Extracellular signal-regulated Kinase (ERK) and c-Jun N-terminal Kinase (JNK) but not p38 Mitogen-Activated Protein Kinase (p38 MAPK), and inhibition of activity of ERK and JNK by U0126 and SP600125 effectively blocked COX-2 and GFAP induction by celecoxib. Celecoxib increased the accumulation of transcription factor AP-1 (composed of phosphorylated c-Jun and c-fos) in the nucleus. Inhibition of AP-1 activity with SR11302 significantly prevented celecoxib-induced COX-2 and GFAP expression. Additionally, the inhibiting activity of ERK and JNK can effectively suppress AP-1 expression and activity induced by celecoxib.</div><div>These findings demonstrated that celecoxib induces COX-2 expression and astrocyte activation through the ERK/JNK/AP-1 signaling pathway, highlighting its potential effect in modulating inflammatory responses in the central nervous system.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"183 ","pages":"Article 105926"},"PeriodicalIF":4.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142902499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

In vitro effects of recombinant human Neuritin on hair cell recovery post-gentamicin injury in SC lineage-tracing models: Involvement of notch and FGFR signaling 重组人神经素对SC谱系追踪模型中庆大霉素损伤后毛细胞恢复的体外影响：Notch和FGFR信号通路的参与

IF 4.4 3区医学

Neurochemistry international Pub Date : 2025-02-01 DOI: 10.1016/j.neuint.2025.105935

Haiyan Wang , Xue Zhang , Fei Gui , Xiaopin Sun , Rong Chen , Guanwu Yin , Yu Hong , Jin Huang , Lei Yang

{"title":"In vitro effects of recombinant human Neuritin on hair cell recovery post-gentamicin injury in SC lineage-tracing models: Involvement of notch and FGFR signaling","authors":"Haiyan Wang , Xue Zhang , Fei Gui , Xiaopin Sun , Rong Chen , Guanwu Yin , Yu Hong , Jin Huang , Lei Yang","doi":"10.1016/j.neuint.2025.105935","DOIUrl":"10.1016/j.neuint.2025.105935","url":null,"abstract":"<div><div>Hair cell (HC) loss, frequently induced by ototoxic agents such as gentamicin, leads to irreversible hearing loss. Because of the restricted regenerative capabilities of the mammalian inner ear, the exploration of therapeutic strategies to restore damaged HCs is critically needed. Recombinant human Neuritin (rhNeuritin), a neurotrophic factor with established roles in promoting cell survival and regeneration across various systems, presents itself as a promising therapeutic candidate for HC repair. In this study, we elucidate the protective effects of rhNeuritin on injured HCs and its capacity to facilitate HC regeneration post-damage. Through the use of cochlear Supporting Cell (SC) lineage-tracing models in neonatal mice, we demonstrate that SC <em>trans</em>-differentiation serves as the origin of HC regeneration following damage. Simultaneously, we uncover that rhNeuritin potentiates the proliferation of SC precursor cells. Mechanistic insights reveal that rhNeuritin-induced cochleae exhibit downregulation of the critical Notch pathway mediator, Hes1, and upregulation of the essential FGFR pathway component Erm, which together may underpin HC regeneration and the proliferation of SC precursors. Notably, rhNeuritin demonstrates significant preservation of HC structural integrity. These findings collectively highlight the therapeutic potential of rhNeuritin in addressing hearing loss resulting from HC damage, thereby opening a new avenue for the restoration of auditory function.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"183 ","pages":"Article 105935"},"PeriodicalIF":4.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142997942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

VNS facilitates the neurological function recovery after ischemia/reperfusion injury by regulating the A1/A2 polarization of astrocytes through the NMU-NMUR2 pathway VNS 通过 NMU-NMUR2 通路调节星形胶质细胞的 A1/A2 极化，从而促进缺血再灌注损伤后神经功能的恢复。

IF 4.4 3区医学

Neurochemistry international Pub Date : 2025-02-01 DOI: 10.1016/j.neuint.2024.105918

Xia Jiang , Wendi Yang , Gang Liu , Hao Tang , Renzi Zhang , Lina Zhang , Changqing Li , Sheng Li

{"title":"VNS facilitates the neurological function recovery after ischemia/reperfusion injury by regulating the A1/A2 polarization of astrocytes through the NMU-NMUR2 pathway","authors":"Xia Jiang , Wendi Yang , Gang Liu , Hao Tang , Renzi Zhang , Lina Zhang , Changqing Li , Sheng Li","doi":"10.1016/j.neuint.2024.105918","DOIUrl":"10.1016/j.neuint.2024.105918","url":null,"abstract":"<div><div>Stroke is the second leading cause of death worldwide. Although conventional treatments such as thrombolysis and mechanical thrombectomy are effective, their narrow therapeutic window limits long-term neurological recovery. Previous studies have shown that vagus nerve stimulation (VNS) enhances neurological recovery after ischemia/reperfusion (I/R) injury, and neuromedin U (NMU) has neuroprotective effects. This study used a mouse model of cerebral I/R injury to investigate the potential mechanisms of NMU in VNS-mediated neurological improvement. The study consisted of two parts: first, assessing the dynamic expression of NMU and NMUR2, which peaked on day 14 post-I/R. NMUR2 was primarily localized in astrocytes, suggesting that the NMU-NMUR2 signaling pathway plays an important role in astrocyte regulation. Next, interventions with VNS, NMU, and R–PSOP + VNS were conducted to evaluate the role of this pathway in VNS-mediated recovery. The results showed that VNS significantly upregulated NMU and NMUR2 expression, which was blocked by the NMUR2 antagonist R–PSOP. VNS and NMU treatment increased the proportion of A2 astrocytes, reduced A1 astrocytes, and enhanced the expression of VEGF and BDNF, all of which were also blocked by R–PSOP. These findings indicate that the \"VNS-NMU-NMUR2-astrocyte A1/A2 polarization-VEGF/BDNF pathway\" plays a crucial role in promoting neurovascular remodeling, axonal and dendritic regeneration, and synaptic plasticity, thereby contributing to functional recovery.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"183 ","pages":"Article 105918"},"PeriodicalIF":4.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142833579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Hydrogen inhalation exerts anti-seizure effects by preventing oxidative stress and inflammation in the hippocampus in a rat model of kainic acid-induced seizures 在kainic酸诱导的大鼠癫痫模型中，氢吸入通过防止海马氧化应激和炎症发挥抗癫痫作用。

IF 4.4 3区医学

Neurochemistry international Pub Date : 2025-02-01 DOI: 10.1016/j.neuint.2024.105925

Tzu-Kang Lin , Ming-Shang Pai , Kun-Chieh Yeh , Chi-Feng Hung , Su-Jane Wang

{"title":"Hydrogen inhalation exerts anti-seizure effects by preventing oxidative stress and inflammation in the hippocampus in a rat model of kainic acid-induced seizures","authors":"Tzu-Kang Lin , Ming-Shang Pai , Kun-Chieh Yeh , Chi-Feng Hung , Su-Jane Wang","doi":"10.1016/j.neuint.2024.105925","DOIUrl":"10.1016/j.neuint.2024.105925","url":null,"abstract":"<div><div>Hydrogen gas (H<sub>2</sub>) is an antioxidant with demonstrated neuroprotective efficacy. In this study, we administered H<sub>2</sub> via inhalation to rats to evaluate its effects on seizures induced by kainic acid (KA) injection and the underlying mechanism. The animals were intraperitoneally injected with KA (15 mg/kg) to induce seizures. H<sub>2</sub> was inhaled 2 h once a day for 5 days before KA administration. The seizure activity was evaluated using Racine's convulsion scale and electroencephalography (EEG). Neuronal cell loss, glial cell activation, and the levels of inflammatory cytokines (TNF-α, IL-1β, IL-6, CCL2, and CCL3), reactive oxygen species (ROS) and nuclear factor erythroid 2-related factor 2 (Nrf2) in the hippocampus were assessed. The cerebral blood flow of the rats was also evaluated. The results revealed that KA-treated rats presented increased seizure intensity; increased neuronal loss and astrocyte activation; increased levels of ROS, TNF-α, IL-1β, IL-6, CCL2, and CCL3; and reduced Nrf2 phosphorylation levels. Pretreatment with H<sub>2</sub> inhalation significantly attenuated seizure intensity; prevented neuronal loss; decreased microglial and astrocytic activation; decreased ROS, TNF-α, IL-1β, IL-6, CCL2 and CCL3 levels; and increased Nrf2 levels. Inhalation of H<sub>2</sub> also prevented the KA-induced decrease in cerebral blood flow. These results suggest that pretreatment with H<sub>2</sub> inhalation ameliorates KA-induced seizures and inhibits the inflammatory response and oxidative stress, which protects neurons.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"183 ","pages":"Article 105925"},"PeriodicalIF":4.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142891174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

The role of mitochondrial remodeling in neurodegenerative diseases 线粒体重塑在神经退行性疾病中的作用。

IF 4.4 3区医学

Neurochemistry international Pub Date : 2025-02-01 DOI: 10.1016/j.neuint.2024.105927

Duanqin Guan , Congmin Liang , Dongyan Zheng , Shizhen Liu , Jiankun Luo , Ziwei Cai , He Zhang , Jialong Chen

{"title":"The role of mitochondrial remodeling in neurodegenerative diseases","authors":"Duanqin Guan , Congmin Liang , Dongyan Zheng , Shizhen Liu , Jiankun Luo , Ziwei Cai , He Zhang , Jialong Chen","doi":"10.1016/j.neuint.2024.105927","DOIUrl":"10.1016/j.neuint.2024.105927","url":null,"abstract":"<div><div>Neurodegenerative diseases are a group of diseases that pose a serious threat to human health, such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD) and Amyotrophic Lateral Sclerosis (ALS). In recent years, it has been found that mitochondrial remodeling plays an important role in the onset and progression of neurodegenerative diseases. Mitochondrial remodeling refers to the dynamic regulatory process of mitochondrial morphology, number and function, which can affect neuronal cell function and survival by regulating mechanisms such as mitochondrial fusion, division, clearance and biosynthesis. Mitochondrial dysfunction is an important intrinsic cause of the pathogenesis of neurodegenerative diseases. Mitochondrial remodeling abnormalities are involved in energy metabolism in neurodegenerative diseases. Pathological changes in mitochondrial function and morphology, as well as interactions with other organelles, can affect the energy metabolism of dopaminergic neurons and participate in the development of neurodegenerative diseases. Since the number of patients with PD and AD has been increasing year by year in recent years, it is extremely important to take effective interventions to significantly reduce the number of morbidities and to improve people's quality of life. More and more researchers have suggested that mitochondrial remodeling and related dynamics may positively affect neurodegenerative diseases in terms of neuronal and self-adaptation to the surrounding environment. Mitochondrial remodeling mainly involves its own fission and fusion, energy metabolism, changes in channels, mitophagy, and interactions with other cellular organelles. This review will provide a systematic summary of the role of mitochondrial remodeling in neurodegenerative diseases, with the aim of providing new ideas and strategies for further research on the treatment of neurodegenerative diseases.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"183 ","pages":"Article 105927"},"PeriodicalIF":4.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142969080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Inhibition of Kv1.1 channels ameliorates Cu(II)-induced microglial activation and cognitive impairment in mice 抑制Kv1.1通道可改善Cu（II）诱导的小鼠小胶质细胞激活和认知障碍。

IF 4.4 3区医学

Neurochemistry international Pub Date : 2025-02-01 DOI: 10.1016/j.neuint.2025.105936

Wenwen Ni , Jiani Ding , Ping Gong , Xiaofang Tan, Juan Li

{"title":"Inhibition of Kv1.1 channels ameliorates Cu(II)-induced microglial activation and cognitive impairment in mice","authors":"Wenwen Ni , Jiani Ding , Ping Gong , Xiaofang Tan, Juan Li","doi":"10.1016/j.neuint.2025.105936","DOIUrl":"10.1016/j.neuint.2025.105936","url":null,"abstract":"<div><div>Microglia-mediated neuroinflammation plays a critical role in neuronal damage in neurodegenerative disorders such as Alzheimer's disease. Evidence shows that voltage-gated potassium (Kv) channels regulate microglial activation. We previously reported that copper dyshomeostasis causes neuronal injury via activating microglia. This study was designed to explore the role of Kv1.1 channels in copper-evoked microglial neuroinflammation. BV-2 microglial cells were treated with Cu(II). DiBAC4(3) was used to measure membrane potential. Microglial activation and neuronal loss were detected by enzyme-linked immunosorbent assay, Western blotting, and immunostaining. Learning and memory function was assessed with Morris water maze task. Cu(II) caused a hyperpolarized membrane potential in microglial cells, an effect abolished by functional Kv1.1 blockade. Blockade of Kv1.1 and knock-down of Kv1.1 with small interfering RNA repressed Cu(II)-induced microglial production of pro-inflammatory mediators. Also, Kv1.1 inhibition attenuated activation of PI3K/Akt-ERK1/2 signaling pathway and production of mitochondrial reactive oxidative species as well as nuclear factor-κB activation in Cu(II)-stimulated microglia. Moreover, the Cu(II)-caused, microglia-mediated neurotoxicity (indicated by reduced neuronal survival and increased dendritic loss) was attenuated by Kv1.1 knock-down. In an <em>in vivo</em> mouse model, hippocampal injection of Cu(II) caused elevated Kv1.1 mRNA (but not other Kv1 channels) expression and enhanced microglial Kv1.1 immunoreactivity in the hippocampus. Furthermore, blockade of Kv1.1 attenuated Cu(II)-induced microglial activation and neuronal dendritic loss in the hippocampus and learning and memory dysfunction. These findings suggest that inhibition of Kv1.1 ameliorates Cu(II)-induced microglial activation and cognitive impairment. Thus, it might represent a potential molecular target for anti-inflammatory therapy of neurodegenerative disorders.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"183 ","pages":"Article 105936"},"PeriodicalIF":4.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142997944","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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