Journal of Molecular Neuroscience最新文献

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MicroRNA Expression Profile Is Altered by Short-Term and Chronic Lithium Treatment in a Rat Model of Depression 抑郁症大鼠模型中的微RNA表达谱因短期和长期锂治疗而改变
IF 2.8 4区 医学
Journal of Molecular Neuroscience Pub Date : 2024-12-15 DOI: 10.1007/s12031-024-02298-0
Maria Kachel, Antonina Dola, Mikołaj Kubiak, Wiktoria Majewska, Joanna Nowakowska, Wojciech Langwiński, Szymon Hryhorowicz, Aleksandra Szczepankiewicz
{"title":"MicroRNA Expression Profile Is Altered by Short-Term and Chronic Lithium Treatment in a Rat Model of Depression","authors":"Maria Kachel,&nbsp;Antonina Dola,&nbsp;Mikołaj Kubiak,&nbsp;Wiktoria Majewska,&nbsp;Joanna Nowakowska,&nbsp;Wojciech Langwiński,&nbsp;Szymon Hryhorowicz,&nbsp;Aleksandra Szczepankiewicz","doi":"10.1007/s12031-024-02298-0","DOIUrl":"10.1007/s12031-024-02298-0","url":null,"abstract":"<div><p>Depression is a common disease that affects 3.8% of the global population. Despite various antidepressant treatments, one-third of patients do not respond to antidepressants, therefore augmentation with mood stabilizers such as lithium may be required in this group. One of the suggested pathomechanisms of depression is the dysregulation of the hypothalamic–pituitary–adrenal (HPA) axis and recent reports showed that microRNAs (miRNA) can impact its activity by epigenetic regulation. We aimed to explore the miRNA expression profile in the depression model and its changes upon short-term and chronic lithium treatment in the rat brain (pituitary, hypothalamus, and hippocampus). We used a chronic mild stress rat model of depression and short- and long-term lithium treatment. The behavior was assessed by an open-field test. The miRNA expression profile in the pituitary was estimated by sequencing and validated in the hypothalamus and hippocampus with qPCR. We found several miRNAs in the pituitary that were significantly altered between CMS-exposed and control rats as well as after short- and long-term lithium treatment. MicroRNAs chosen for validation in the hypothalamus and hippocampus (rno-miR-146a-5p, rno-miR-127-3p) showed no significant changes in expression. We performed in silico analysis and estimated potential pathways involved in lithium action for miRNAs differentially expressed in the pituitary at different time points. Specific microRNA subsets showed altered expression in the pituitary in depression model upon short- and long-term lithium treatment. We identified that biological pathways of target genes for these altered miRNAs differ, with the Foxo pathway potentially involved in disease development.</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"74 4","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142821386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Exploring the Role of Chemokine-Related Gene Deregulation and Immune Infiltration in Ischemic Stroke: Insights into CXCL16 and SEMA3E as Potential Biomarkers 探索趋化因子相关基因调控和免疫浸润在缺血性卒中中的作用:CXCL16和SEMA3E作为潜在生物标志物的见解
IF 2.8 4区 医学
Journal of Molecular Neuroscience Pub Date : 2024-12-12 DOI: 10.1007/s12031-024-02295-3
Tingting Yu, Peng Jiang
{"title":"Exploring the Role of Chemokine-Related Gene Deregulation and Immune Infiltration in Ischemic Stroke: Insights into CXCL16 and SEMA3E as Potential Biomarkers","authors":"Tingting Yu,&nbsp;Peng Jiang","doi":"10.1007/s12031-024-02295-3","DOIUrl":"10.1007/s12031-024-02295-3","url":null,"abstract":"<div><p>Ischemic stroke is a leading cause of mortality and disability globally. Understanding the role of chemokine-related differently expressed genes (CDGs) in ischemic stroke pathophysiology is essential for advancing diagnostic and therapeutic strategies. We conducted comprehensive analyses using the GSE16561 dataset: chemokine pathway enrichment via GSVA, differential expression of 12 CDGs, Pearson correlation, and functional enrichment analyses (GO and KEGG). Machine learning algorithms were employed to develop diagnostic models, evaluated using ROC curve analysis. A nomogram was constructed and validated with independent datasets (GSE58294). Gene set enrichment analysis (GSEA) and immuno-infiltration analysis were also performed. Chemokine pathway scores were significantly elevated in ischemic stroke, indicating their potential involvement. Logistic regression emerged as the most effective diagnostic model, with CXCL16 and SEMA3E as significant biomarkers. The nomogram exhibited high discriminatory ability (AUC = 0.964), well-calibrated predictions, and clinical utility across datasets. GSEA highlighted key biological pathways associated with CXCL16 and SEMA3E. Immuno-infiltration analysis revealed significant differences in immune cell infiltration between control and ischemic stroke groups, with distinct correlations between CXCL16 and SEMA3E expression and immune cell populations. This study highlights the deregulation of CDGs in ischemic stroke and their implications in critical biological processes. CXCL16 and SEMA3E are identified as key biomarkers with potential diagnostic utility. Insights from gene set enrichment and immuno-infiltration analyses provide mechanistic understanding, suggesting novel therapeutic targets and enhancing clinical decision-making in ischemic stroke management.</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"74 4","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142811181","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Advanced Glycation End Products in Neurodegenerative Diseases 神经退行性疾病的晚期糖基化终产物
IF 2.8 4区 医学
Journal of Molecular Neuroscience Pub Date : 2024-12-10 DOI: 10.1007/s12031-024-02297-1
Cibin T. Raghavan
{"title":"Advanced Glycation End Products in Neurodegenerative Diseases","authors":"Cibin T. Raghavan","doi":"10.1007/s12031-024-02297-1","DOIUrl":"10.1007/s12031-024-02297-1","url":null,"abstract":"<div><p>Advanced glycation end products (AGEs) have attracted interest as therapeutic targets for neurodegenerative diseases. AGEs facilitate the onset and progression of various neurogenerative disorders due to their ability to promote cross-linking and aggregation of proteins. Further, the interaction between AGEs and receptor for AGEs (RAGE) activates neuroinflammatory, oxidative stress and excitotoxicity processes that contribute to neuronal cell death. Various therapeutic efforts have targeted lowering the production of AGEs, inhibiting RAGE or inhibiting some of the processes of the AGE-RAGE axis as potential treatments for these disorders. Whereas effective treatments for many neurodegenerative disorders remain elusive, such efforts offer promise to slow the progression of diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD) and Huntington’s disease (HD).</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"74 4","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142798260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Melatonin’s Impact on Cytokine Storm and Modulation of Purinergic Receptors for COVID-19 Prognosis: A Mental Health Perspective 褪黑素对细胞因子风暴和嘌呤能受体调节对COVID-19预后的影响:心理健康视角
IF 2.8 4区 医学
Journal of Molecular Neuroscience Pub Date : 2024-12-05 DOI: 10.1007/s12031-024-02292-6
Amanda Gollo Bertollo, Joana Bortolanza Dalazen, Joana Vitória Cassol, Mariélly Braun Hellmann, Tiago Libério Mota, Zuleide Maria Ignácio, Margarete Dulce Bagatini
{"title":"Melatonin’s Impact on Cytokine Storm and Modulation of Purinergic Receptors for COVID-19 Prognosis: A Mental Health Perspective","authors":"Amanda Gollo Bertollo,&nbsp;Joana Bortolanza Dalazen,&nbsp;Joana Vitória Cassol,&nbsp;Mariélly Braun Hellmann,&nbsp;Tiago Libério Mota,&nbsp;Zuleide Maria Ignácio,&nbsp;Margarete Dulce Bagatini","doi":"10.1007/s12031-024-02292-6","DOIUrl":"10.1007/s12031-024-02292-6","url":null,"abstract":"<div><p>In 2019, coronavirus disease 2019 (COVID-19) started a global health crisis and was associated with high rates of depression and anxiety. Both mental disorders and COVID-19 exhibit similarities in pathophysiology, characterized by immune system overactivation, involvement of the purinergic system, and oxidative stress, besides additional factors and systems likely contributing to the complexities of these conditions. The purinergic system contributes to the disease-influenced immune response, an essential strategy for controlling pathophysiological effects. In this context, the hormone melatonin emerges as a substance that can modulate the purinergic system and contribute positively to the pathophysiology of SARS-CoV-2 infection and associated mental disorders. Melatonin is a hormone that regulates the body’s circadian rhythms, plays an essential role in regulating sleep and mood, and modulates the purinergic system. Recent studies suggest melatonin’s anti-inflammatory and antioxidant properties may benefit COVID-19. This review explores melatonin’s impact on inflammatory cytokine storm in COVID-19 through purinergic system modulation.</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"74 4","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142778524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Effect of Prednisolone on Clinical and Cytokine mRNA Profiling in Complex Regional Pain Syndrome 强的松龙对复杂局部疼痛综合征临床及细胞因子mRNA谱的影响
IF 2.8 4区 医学
Journal of Molecular Neuroscience Pub Date : 2024-12-04 DOI: 10.1007/s12031-024-02290-8
Jayantee Kalita, Ruchi Shukla, Prakash C. Pandey
{"title":"Effect of Prednisolone on Clinical and Cytokine mRNA Profiling in Complex Regional Pain Syndrome","authors":"Jayantee Kalita,&nbsp;Ruchi Shukla,&nbsp;Prakash C. Pandey","doi":"10.1007/s12031-024-02290-8","DOIUrl":"10.1007/s12031-024-02290-8","url":null,"abstract":"<div><p>The cardinal clinical features of complex regional pain syndrome type I (CRPS-I) are pain, edema, autonomic changes, and limitation of motoric movement, which may indicate the role of inflammation and cytokines. We report the effect of prednisolone on the clinical severity and mRNA profiling of proinflammatory (tumor necrosis factor (TNF)-α and interleukin (IL)-2) and anti-inflammatory cytokines (IL-10 and transforming growth factor (TGF)-β) in the patient with CRPS-I. Thirty-nine patients with CRPS-I of shoulder joint were enrolled. Their CRPS, Visual Analog Scale (VAS) and Daily Sleep Interference Scale (DSIS) scores were recorded. TNF-α, IL-2, IL-10, and TGF-β gene expressions at mRNA of whole blood were measured by reverse transcriptase polymerase chain reaction. Patients were randomized to prednisolone 20 mg or 40 mg using 1: 1 randomization. The primary outcome was change in VAS score, and secondary outcomes were change in CRPS and DSIS scores at 1 month. Side effects were noted. The patients had increased expressions of TNF-α (<i>p</i> &lt; 0.001) and IL-2 (<i>p</i> &lt; 0.001) and reduced IL-10 (<i>p</i> &lt; 0.01) mRNA compared to the healthy controls. The baseline characteristics were matched between the two treatment arms. At 1 month, CRPS, VAS, and DSIS scores improved significantly compared to baseline, which paralleled with improvement in IL-10 (<i>p</i> &lt; 0.032) and reduction in TNF-α (<i>p</i> = 0.046). The improvement in clinical and biomarkers was similar in prednisolone 20 mg and 40 mg arms. None had to be withdrawn due to severe side effects. Future study in larger cohort may validate these findings.</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"74 4","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142778361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Valproate Administration to Adult 5xFAD Mice Upregulates Expression of Neprilysin and Improves Olfaction and Memory 给成年 5xFAD 小鼠注射丙戊酸钠可上调肾蛋白酶的表达并改善嗅觉和记忆。
IF 2.8 4区 医学
Journal of Molecular Neuroscience Pub Date : 2024-11-16 DOI: 10.1007/s12031-024-02287-3
Dmitrii S. Vasilev, Nadezhda M. Dubrovskaya, Natalia L. Tumanova, Aleksandr N. Tursunov, Natalia N. Nalivaeva
{"title":"Valproate Administration to Adult 5xFAD Mice Upregulates Expression of Neprilysin and Improves Olfaction and Memory","authors":"Dmitrii S. Vasilev,&nbsp;Nadezhda M. Dubrovskaya,&nbsp;Natalia L. Tumanova,&nbsp;Aleksandr N. Tursunov,&nbsp;Natalia N. Nalivaeva","doi":"10.1007/s12031-024-02287-3","DOIUrl":"10.1007/s12031-024-02287-3","url":null,"abstract":"<div><p>It is well known that the development of neurodegeneration, and especially Alzheimer’s disease (AD), is often accompanied by impaired olfaction which precedes memory loss. A neuropeptidase neprilysin (NEP)—a principal amyloid-degrading enzyme in the brain—was also shown to be involved in olfactory signalling. Previously we have demonstrated that 5xFAD mice develop olfactory deficit by the age of 6 months which correlated with reduced NEP expression in the brain areas involved in olfactory signalling. The aim of this study was to analyse the effect of administration of a histone deacetylase inhibitor, valproic acid (VA), to adult 5xFAD mice on their olfaction and memory as well as on brain morphology and NEP expression in the parietal cortex (PC) and hippocampus (Hip). The data obtained demonstrated that administration of VA to 7-month-old mice (200 mg/kg of body weight) for 28 days resulted in improvement of their memory in the Morris water maze as well as olfaction in the odor preference and food search tests. This correlated with increased expression of NEP in the PC and Hip as well as a reduced number of amyloid plaques in these brain areas. This strongly suggests that NEP can be considered an important therapeutic target not only in AD but also in olfactory loss.</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"74 4","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142643620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Investigation of Association Between Expression of DYX1C1, KIAA0319, and ROBO1 Genes and Specific Learning Disorder in Children and Adolescents 儿童和青少年中 DYX1C1、KIAA0319 和 ROBO1 基因的表达与特殊学习障碍之间的关联调查
IF 2.8 4区 医学
Journal of Molecular Neuroscience Pub Date : 2024-11-15 DOI: 10.1007/s12031-024-02288-2
Burcu Bayyurt, Nil Özbilüm Şahin, Cansu Mercan Işık
{"title":"Investigation of Association Between Expression of DYX1C1, KIAA0319, and ROBO1 Genes and Specific Learning Disorder in Children and Adolescents","authors":"Burcu Bayyurt,&nbsp;Nil Özbilüm Şahin,&nbsp;Cansu Mercan Işık","doi":"10.1007/s12031-024-02288-2","DOIUrl":"10.1007/s12031-024-02288-2","url":null,"abstract":"<div><p>Specific learning disorder (SLD) is prevalent worldwide and is a complex disorder with variable symptoms and significant differences among individuals. Epigenetic markers may alter susceptibility to neurodevelopmental disorders (NDDs). Aberrant expression of protein-coding (mRNA) genes in this pathology shows that the detection of epigenetic molecular biomarkers is of increasing importance in the diagnosis and treatment of individuals with SLD. We compared gene expression level of <i>dyslexia susceptibility 1 candidate gene 1</i> (<i>DYX1C1</i>), <i>dyslexia-associated protein KIAA0319</i> (<i>KIAA0319</i>), and <i>roundabout guidance receptor 1</i> (<i>ROBO1</i>) between children with SLD and healthy children by performing quantitative polymerase chain reaction (qPCR). In addition, we evaluated these gene expressions of severe children with SLD compared to non-severe and male SLD children compared to females. The expression of the <i>DYX1C1</i>, <i>KIAA0319</i>, and <i>ROBO1</i> genes was statistically significantly upregulated in children with SLD (<i>P</i> &lt; 0.05*). <i>DYX1C1</i> was also upregulated in severe SLD children (<i>P</i> = 0.03*). In addition, <i>KIAA0319</i> and <i>ROBO1</i> genes were differentially expressed in male SLD children compared to females (<i>P</i> &lt; 0.05*). Furthermore, we found that <i>DYX1C1</i> and <i>ROBO1</i> genes significantly affect the likelihood of the SLD (respectively, <i>P</i> &lt; 0.001** and <i>P</i> = 0.007*). We expect that the findings provided from this study may contribute to the determination expression level of the relevant genes in the diagnosis, prognosis, and treatment of SLD. In addition, our findings could be a guide for future epigenetics studies on the use of the <i>DYX1C1</i>, <i>KIAA0319</i>, and <i>ROBO1</i> in therapeutic applications in the SLD.</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"74 4","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142611764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Role and Interplay of Different Signaling Pathways Involved in Sciatic Nerve Regeneration 参与坐骨神经再生的不同信号通路的作用和相互作用
IF 2.8 4区 医学
Journal of Molecular Neuroscience Pub Date : 2024-11-12 DOI: 10.1007/s12031-024-02286-4
Saeedeh Zare Jalise, Sina Habibi, Leyla Fath-Bayati, Mohammad Amin Habibi, Shima Ababzadeh, Faezeh Hosseinzadeh
{"title":"Role and Interplay of Different Signaling Pathways Involved in Sciatic Nerve Regeneration","authors":"Saeedeh Zare Jalise,&nbsp;Sina Habibi,&nbsp;Leyla Fath-Bayati,&nbsp;Mohammad Amin Habibi,&nbsp;Shima Ababzadeh,&nbsp;Faezeh Hosseinzadeh","doi":"10.1007/s12031-024-02286-4","DOIUrl":"10.1007/s12031-024-02286-4","url":null,"abstract":"<div><p>Regeneration of the sciatic nerve is a sophisticated process that involves the interplay of several signaling pathways that orchestrate the cellular responses critical to regeneration. Among the key pathways are the mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinase (PI3K)/AKT, cyclic adenosine monophosphate (cAMP), and Janus kinase/signal transducers and transcription activators (JAK/STAT) pathways. In particular, the cAMP pathway modulates neuronal survival and axonal regrowth. It influences various cellular behaviors and gene expression that are essential for nerve regeneration. MAPK is indispensable for Schwann cell differentiation and myelination, whereas PI3K/AKT is integral to the transcription, translation, and cell survival processes that are vital for nerve regeneration. Furthermore, GTP-binding proteins, including those of the Ras homolog gene family (Rho), regulate neural cell adhesion, migration, and survival. Notch signaling also appears to be effective in the early stages of nerve regeneration and in preventing skeletal muscle fibrosis after injury. Understanding the intricate mechanisms and interactions of these pathways is vital for the development of effective therapeutic strategies for sciatic nerve injuries. This review underscores the need for further research to fill existing knowledge gaps and improve therapeutic outcomes.</p><h3>Graphical Abstract</h3><div><figure><div><div><picture><source><img></source></picture></div></div></figure></div></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"74 4","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142600644","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Mitophagy Unveiled: Exploring the Nexus of Mitochondrial Health and Neuroendocrinopathy 揭开线粒体吞噬的神秘面纱探索线粒体健康与神经内分泌病变的联系
IF 2.8 4区 医学
Journal of Molecular Neuroscience Pub Date : 2024-11-08 DOI: 10.1007/s12031-024-02280-w
Mega Obukohwo Oyovwi, Emeka Williams Ugwuishi, Onoriode Andrew Udi, Gregory Joseph Uchechukwu
{"title":"Mitophagy Unveiled: Exploring the Nexus of Mitochondrial Health and Neuroendocrinopathy","authors":"Mega Obukohwo Oyovwi,&nbsp;Emeka Williams Ugwuishi,&nbsp;Onoriode Andrew Udi,&nbsp;Gregory Joseph Uchechukwu","doi":"10.1007/s12031-024-02280-w","DOIUrl":"10.1007/s12031-024-02280-w","url":null,"abstract":"<div><p>Mitochondria play a pivotal role in cellular metabolism, energy production, and apoptotic signaling, making mitophagy, the selective degradation of damaged mitochondria, crucial for mitochondrial health. Dysregulation of mitophagy has been implicated in various neuroendocrinopathies, yet the mechanisms linking these processes remain poorly understood. This review aims to explore the intersection between mitophagy and neuroendocrinopathy, addressing the critical gaps in knowledge regarding how mitochondrial dysfunction may contribute to the pathophysiology of neuroendocrine disorders. We conducted a comprehensive literature review of studies published on mitophagy and neuroendocrinopathies, focusing on data that elucidate the pathways involved and the clinical implications of mitochondrial health in neuroendocrine contexts. Our findings indicate that altered mitophagy may lead to the accumulation of dysfunctional mitochondria, contributing to neuroendocrine dysregulation. We present evidence linking impaired mitochondrial clearance to disease models of conditions such as metabolic syndrome, depression, and stress-related disorders, highlighting the potential for therapeutic interventions targeting mitophagy. While significant advances have been made in understanding mitochondrial biology, the direct interplay between mitophagy and neuroendocrinopathies remains underexplored. This review underscores the necessity for further research to elucidate these connections, which may offer novel insights into disease mechanisms and therapeutic strategies for treating maladaptive neuroendocrine responses.</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"74 4","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142596088","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
Antisecretory Factor 16 (AF16): A Promising Avenue for the Treatment of Traumatic Brain Injury—An In Vitro Model Approach 抗分泌因子 16 (AF16):治疗创伤性脑损伤的希望之路--一种体外模型方法。
IF 2.8 4区 医学
Journal of Molecular Neuroscience Pub Date : 2024-11-07 DOI: 10.1007/s12031-024-02268-6
Nicola Vahrmeijer, Jurgen Kriel, Bradley M. Harrington, Anton Du Preez van Staden, Adriaan Johannes Vlok, Lize Engelbrecht, Andre Du Toit, Ben Loos
{"title":"Antisecretory Factor 16 (AF16): A Promising Avenue for the Treatment of Traumatic Brain Injury—An In Vitro Model Approach","authors":"Nicola Vahrmeijer,&nbsp;Jurgen Kriel,&nbsp;Bradley M. Harrington,&nbsp;Anton Du Preez van Staden,&nbsp;Adriaan Johannes Vlok,&nbsp;Lize Engelbrecht,&nbsp;Andre Du Toit,&nbsp;Ben Loos","doi":"10.1007/s12031-024-02268-6","DOIUrl":"10.1007/s12031-024-02268-6","url":null,"abstract":"<div><p>Traumatic brain injury (TBI) is caused by an external mechanical force to the head, resulting in abnormal brain functioning and clinical manifestations. Antisecretory factor (AF16) is a potential therapeutic agent for TBI treatment due to its ability to inhibit fluid secretion and decrease inflammation, intracranial pressure, and interstitial fluid build-up, key hallmarks presented in TBI. Here, we investigated the effect of AF16 in an in vitro model of neuronal injury, as well as its impact on key components of the autophagy pathway and mitochondrial dynamics. N2A<sup>wt</sup> cells were treated with AF16, injured using a scratch assay, and analysed using confocal microscopy, correlative light and electron microscopy (CLEM), flow cytometry, and western blotting. Our results reveal that AF16 enhances autophagy activity, regulates mitochondrial dynamics, and provides protection as early as 6 h post-injury. Fluorescently labelled AF16 was observed to localise to lysosomes and the autophagy compartment, suggesting a role for autophagy and mitochondrial quality control in conferring AF16-associated neuronal protection. This study concludes that AF16 has potential as a therapeutic agent for TBI treatment through is regulation of autophagy and mitochondrial dynamics.</p></div>","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"74 4","pages":""},"PeriodicalIF":2.8,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s12031-024-02268-6.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142589350","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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
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