Current Neuropharmacology最新文献

{"title":"Olanzapine Induces Adipogenesis and Glucose Uptake by Activating Glycolysis and Synergizing with the PI3K-AKT Pathway.","authors":"Shen Li, Yun Fu, Wanyao Wang, Jiali Qiu, Yepei Huang, Xuemin Li, Ke Yang, Xiawen Yu, Yanyan Ma, Yuan Zhang, Miaomiao Zhang, Jie Li, Wei-Dong Li","doi":"10.2174/1570159X22666240815120547","DOIUrl":"https://doi.org/10.2174/1570159X22666240815120547","url":null,"abstract":"<p><strong>Background: </strong>Administration of olanzapine (OLA) is closely associated with obesity and glycolipid abnormalities in patients with schizophrenia (SCZ), although the exact molecular mecha- nisms remain elusive.</p><p><strong>Objective: </strong>We conducted comprehensive animal and molecular experiments to elucidate the mecha- nisms underlying OLA-induced weight gain.</p><p><strong>Methods: </strong>We investigated the mechanisms of OLA-induced adipogenesis and lipid storage by em- ploying a real-time ATP production rate assay, glucose uptake test, and reactive oxygen species (ROS) detection in 3T3-L1 cells and AMSCs. Rodent models were treated with OLA using various interven- tion durations, dietary patterns (normal diets/western diets), and drug doses. We assessed body weight, epididymal and liver fat levels, and metabolic markers in both male and female mice.</p><p><strong>Results: </strong>OLA accelerates adipogenesis by directly activating glycolysis and its downstream PI3K sig- naling pathway in differentiated adipocytes. OLA promotes glucose uptake in differentiated 3T3-L1 preadipocytes. In mouse models with normal glycolipid metabolism, OLA administration failed to in- crease food intake and weight gain despite elevated GAPDH expression, a marker related to glycolysis and PI3K-AKT. This supports the notion that glycolysis plays a significant role in OLA-induced met- abolic dysfunction.</p><p><strong>Conclusion: </strong>OLA induces glycolysis and activates the downstream PI3K-AKT signaling pathway, thereby promoting adipogenesis.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2024-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141987516","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}

{"title":"MiRNA Dysregulation in Brain Injury: An In Silico Study to Clarify the Role of a MiRNA Set.","authors":"Francesco Sessa, Cristoforo Pomara, Flavia Schembari, Massimiliano Esposito, Emanuele Capasso, Mauro Pesaresi, Eduardo Osuna, Efehan Ulas, Christian Zammit, Monica Salerno","doi":"10.2174/1570159X22666240808124427","DOIUrl":"https://doi.org/10.2174/1570159X22666240808124427","url":null,"abstract":"<p><strong>Background: </strong>The identification of specific circulating miRNAs has been proposed as a valuable tool for elucidating the pathophysiology of brain damage or injury and predicting patient outcomes.</p><p><strong>Objective: </strong>This study aims to apply several bioinformatic tools in order to clarify miRNA interactions with potential genes involved in brain injury, emphasizing the need of using a computational approach to determine the most likely correlations between miRNAs and target genes. Specifically, this study centers on elucidating the roles of miR-34b, miR-34c, miR-135a, miR-200c, and miR-451a.</p><p><strong>Methods: </strong>After a careful evaluation of different software available (analyzing the strengths and limitations), we applied three tools, one to perform an analysis of the validated targets (miRTarBase), and two to evaluate functional annotations (miRBase and TAM 2.0).</p><p><strong>Results: </strong>Research findings indicate elevated levels of miR-135a and miR-34b in patients with traumatic brain injury (TBI) within the first day post-injury, while miR-200c and miR-34c were found to be upregulated after 7 days. Moreover, miR-451a and miR-135a were found overexpressed in the serum, while miRNAs 34b, 34c, and 200c, had lower serum levels at baseline post brain injury.</p><p><strong>Conclusion: </strong>This study emphasizes the use of computational methods in determining the most likely relationships between miRNAs and target genes by investigating several bioinformatic techniques to elucidate miRNA interactions with potential genes. Specifically, this study focuses on the functions of miR-34b, miR-34c, miR-135a, miR-200c, and miR-451a, providing an up-to-date overview and suggesting future research directions for identifying theranomiRNAs related to brain injury, both at the tissue and serum levels.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2024-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141916308","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}

{"title":"Bibliometric Analysis of Alzheimer's Disease and Depression.","authors":"Sixin Li, Qian Zhang, Jian Liu, Nan Zhang, Xinyu Li, Ying Liu, Huiwen Qiu, Jing Li, Hui Cao","doi":"10.2174/1570159X22666240730154834","DOIUrl":"https://doi.org/10.2174/1570159X22666240730154834","url":null,"abstract":"<p><strong>Background: </strong>The link between Alzheimer's disease and depression has been confirmed by clinical and epidemiological research. Therefore, our study examined the literary landscape and prevalent themes in depression-related research works on Alzheimer's disease through bibliometric analysis.</p><p><strong>Methods: </strong>Relevant literature was identified from the Web of Science core collection. Bibliometric parameters were extracted, and the major contributors were defined in terms of countries, institutions, authors, and articles using Microsoft Excel 2019 and VOSviewer. VOSviewer and CiteSpace were employed to visualize the scientific networks and seminal topics.</p><p><strong>Results: </strong>The analysis of literature utilised 10,553 articles published from 1991 until 2023. The three countries or regions with the most publications were spread across the United States, China, and England. The University of Toronto and the University of Pittsburgh were the major contributors to the institutions. Lyketsos, Constantine G., Cummings, JL were found to make outstanding contributions. Journal of Alzheimer's Disease was identified as the most productive journal. Furthermore, \"Alzheimer's\", \"depression\", \"dementia\", and \"mild cognitive decline\" were the main topics of discussion during this period.</p><p><strong>Limitations: </strong>Data were searched from a single database to become compatible with VOSviewer and CiteSpace, leading to a selection bias. Manuscripts in English were considered, leading to a language bias.</p><p><strong>Conclusion: </strong>Articles on \"Alzheimer's\" and \"depression\" displayed an upward trend. The prevalent themes addressed were the mechanisms of depression-associated Alzheimer's disease, the identification of depression and cognitive decline in the early stages of Alzheimer's, alleviating depression and improving life quality in Alzheimer's patients and their caregivers, and diagnosing and treating neuropsychiatric symptoms in Alzheimer. Future research on these hot topics would promote understanding in this field.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2024-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141874437","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}

{"title":"Notch Signaling in Central Nervous System: From Cellular Development to Multiple Sclerosis Disease.","authors":"Hamid Askari, Fatemeh Rabiei, Giuseppe Biagini, Masoomeh Yahyazadeh, Maryam Ghasemi-Kasman","doi":"10.2174/1570159X22666240731114906","DOIUrl":"https://doi.org/10.2174/1570159X22666240731114906","url":null,"abstract":"<p><strong>Introduction/objective: </strong>Multiple sclerosis (MS), is characterized by autoimmune-driven neuroinflammation, axonal degeneration, and demyelination. This study aimed to explore the therapeutic potential of targeting Notch signaling within the central nervous system (CNS) in the context of MS. Understanding the intricate roles of Notch signaling could pave the way for targeted interventions to mitigate MS progression.</p><p><strong>Methods: </strong>A comprehensive literature review was conducted using databases such as PubMed, Web of Science, and Scopus. Keywords such as \"Notch signaling,\" \"neuroglial interactions,\" and \"MS\" were used. The selection criteria included relevance to neuroglial interactions, peer-reviewed publications, and studies involving animal models of MS.</p><p><strong>Results: </strong>This review highlights the diverse functions of Notch signaling in CNS development, including its regulation of neural stem cell differentiation into neurons, astrocytes, and oligodendrocytes. In the context of MS, Notch signaling has emerged as a promising therapeutic target, exhibiting positive impacts on neuroprotection and remyelination. However, its intricate nature within the CNS necessitates precise modulation for therapeutic efficacy.</p><p><strong>Conclusion: </strong>This study provides a comprehensive overview of the potential therapeutic role of Notch signaling in MS. The findings underscore the significance of Notch modulation for neuroprotection and remyelination, emphasizing the need for precision in therapeutic interventions. Further research is imperative to elucidate the specific underlying mechanisms involved, which will provide a foundation for targeted therapeutic strategies for the management of MS and related neurodegenerative disorders.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2024-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142003829","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}

{"title":"Vitamin B6 Via p-JNK/Nrf-2/NF-κB Signaling Ameliorates Cadmium Chloride-Induced Oxidative Stress Mediated Memory Deficits in Mice Hippocampus.","authors":"Abdul Nasir, Mujeeb Ur Rahman, Manzar Khan, Muhammad Zahid, Muhammad Shahab, Hongjun Jiao, Amir Zeb, Shahid Ali Shah, Haroon Khan","doi":"10.2174/1570159X22999240730154422","DOIUrl":"https://doi.org/10.2174/1570159X22999240730154422","url":null,"abstract":"<p><strong>Background: </strong>Cadmium chloride (Cd) is a pervasive environmental heavy metal pollutant linked to mitochondrial dysfunction, memory loss, and genetic disorders, particularly in the context of neurodegenerative diseases like Alzheimer's disease (AD).</p><p><strong>Methods: </strong>This study investigated the neurotherapeutic potential of vitamin B6 (Vit. B6) in mitigating Cd-induced oxidative stress and neuroinflammation-mediated synaptic and memory dysfunction. Adult albino mice were divided into four groups: Control (saline-treated), Cd-treated, Cd+Vit. B6- treated, and Vit. B6 alone-treated. Cd and Vit. B6 were administered intraperitoneally, and behavioral tests (Morris Water Maze, Y-Maze) were conducted. Subsequently, western blotting, antioxidant assays, blood glucose, and hyperlipidemia assessments were performed.</p><p><strong>Results: </strong>Cd-treated mice exhibited impaired cognitive function, while Cd+Vit. B6-treated mice showed significant improvement. Cd-induced neurotoxic effects, including oxidative stress and neuroinflammation, were observed, along with disruptions in synaptic proteins (SYP and PSD95) and activation of p-JNK. Vit. B6 administration mitigated these effects, restoring synaptic and memory deficits. Molecular docking and MD simulation studies confirmed Vit. B6's inhibitory effect on IL-1β, NRF2, and p-JNK proteins.</p><p><strong>Conclusion: </strong>These results highlight Vit. B6 as a safe therapeutic supplement to mitigate neurodegenerative disorders, emphasizing the importance of assessing nutritional interventions for combating environmental neurotoxicity in the interest of public health.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2024-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141874382","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}

{"title":"Deciphering the Causality between Gut Microbiota Dysbiosis and Poisoning by Narcotics and Psychodysleptics: A Mendelian Randomization Analysis.","authors":"Ning Wang, Zhenbo Su","doi":"10.2174/1570159X22999240729092453","DOIUrl":"https://doi.org/10.2174/1570159X22999240729092453","url":null,"abstract":"<p><strong>Background: </strong>This study investigates the connection between gut microbiota and poisoning caused by narcotics and psychodysleptics, using Mendelian randomization (MR) to explore possible causal relationships.</p><p><strong>Methods: </strong>The study employed the MR analysis, leveraging genetic variants as instrumental variables to facilitate robust causal inference. Data for gut microbiota was extracted from the MiBioGen study, integrating genome-wide genotyping data with 16S fecal microbiota profiles. Outcome metrics were based on the Finngen study. Genetic instruments were meticulously extracted based on stringent criteria, and harmonized with SNP outcomes associated with \"Poisoning by narcotics and psychodysleptics [hallucinogens]\". The inverse-variance weighted (IVW) method was utilized for MR analysis, supplemented by sensitivity analyses including MR-Egger Regression, Weighted Median Approach, and Leave-One-Out Cross-Validation.</p><p><strong>Results: </strong>Among various microbial groups, nine showed significant statistical links. Specifically, Class Negativicutes (OR 5.68, 95% CI 2.13-15.16, p = 0.0005) and Order Selenomonadales (OR 5.68, 95% CI 2.13-15.16, p = 0.0005) were notably associated. These findings were consistent across different sensitivity analyses.</p><p><strong>Conclusion: </strong>The relationship between gut microbiota and the adverse effects of narcotics and psychodysleptics is an emerging area of research. Our MR study identifies certain microbes that might influence the body's response to these substances. These insights could help in predicting and treating the effects of narcotics and psychodysleptics in the future.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2024-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141855104","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}

{"title":"Ghrelin, Neuroinflammation, Oxidative Stress, and Mood Disorders: What Are the Connections?","authors":"Jessica Mingardi, Ramona Meanti, Caterina Paoli, Carlo Cifani, Antonio Torsello, Maurizio Popoli, Laura Musazzi","doi":"10.2174/1570159X22999240722095039","DOIUrl":"https://doi.org/10.2174/1570159X22999240722095039","url":null,"abstract":"<p><p>Ghrelin is a gut peptide hormone associated with feeding behavior and energy homeostasis. Acylated ghrelin binds to the growth hormone secretagogue receptor 1a subtype (GHS-R1a) in the hippocampus, leading to GH release from the anterior pituitary. However, in recent years, ghrelin and its receptor have also been implicated in other processes, including the regulation of cardiomyocyte function, muscle trophism, and bone metabolism. Moreover, GHS-R1a is distributed throughout the brain and is expressed in brain areas that regulate the stress response and emotional behavior. Consistently, a growing body of evidence supports the role of ghrelin in regulating stress response and mood. Stress has consistently been shown to increase ghrelin levels, and despite some inconsistencies, both human and rodent studies suggested antidepressant effects of ghrelin. Nevertheless, the precise mechanism by which ghrelin influences stress response and mood remains largely unknown. Intriguingly, ghrelin and GHS-R1a were consistently reported to exert anti-inflammatory, antioxidant, and neurotrophic effects both in vivo and in vitro, although this has never been directly assessed in relation to psychopathology. In the present review we will discuss available literature linking ghrelin with the stress response and depressive-like behavior in animal models as well as evidence describing the interplay between ghrelin and neuroinflammation/oxidative stress. Although further studies are required to understand the mechanisms involved in the action of ghrelin on mood, we hypothesize that the antiinflammatory and anti-oxidative properties of ghrelin may give a key contribution.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2024-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141747684","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}

{"title":"Time- and Region-specific Effect of Vortioxetine on Central LPS-induced Transcriptional Regulation of NLRP3 Inflammasome.","authors":"Miriam Ciani, Giovanna Rigillo, Cristina Benatti, Luca Pani, Johanna M C Blom, Nicoletta Brunello, Fabio Tascedda, Silvia Alboni","doi":"10.2174/1570159X22666240705143649","DOIUrl":"https://doi.org/10.2174/1570159X22666240705143649","url":null,"abstract":"<p><strong>Background: </strong>Inflammasome overactivation, multiprotein complexes that trigger inflammatory responses, plays a critical role in Major Depressive Disorder (MDD) pathogenesis and treatment responses. Indeed, different antidepressants alleviate depression-related behaviours by specifically counteracting the NLRP3 inflammasome signalling pathway. The immunomodulatory effects of vortioxetine (VTX), a multimodal antidepressant with cognitive benefits, were recently revealed to counter memory impairment induced by a peripheral lipopolysaccharide (LPS) injection 24 hours (h) postchallenge.</p><p><strong>Methods: </strong>The potential link between VTX and NLRP3, along with other inflammasomes, remains unexplored. Hence, adult C57BL/6J male mice (n = 73) were fed with a standard or VTX-enriched diet (600 mg/kg of food, 28 days), injected with LPS (830 μg/kg) or saline, and sacrificed 6/24 h post-LPS. At these time-points, transcriptional effects of LPS and VTX's on NLRP3, NLRP1, NLRC4, AIM2 (inflammasomes), ASC and CASP1 (related subunits) and NEK7 mediator (NLRP3 regulator) were assessed in dorsal and ventral hippocampal subregions, frontal-prefrontal cortex and hypothalamus, brain regions serving behavioural-cognitive functions impaired in MDD.</p><p><strong>Results: </strong>Varied expression patterns of inflammasomes were revealed, with long-term NLRP3 and ASC transcriptional changes observed in response to LPS. It was discovered that VTX counteracted the LPS-mediated NLRP3 and ASC upregulation in memory-related brain areas like the dorsal hippocampus at 24 h time-point, potentially via regulating NEK7 expression. No VTX-mediated transcriptional effects were observed on other inflammasomes, reinforcing a potentially specific modulation on the NLRP3 inflammasome signalling pathway.</p><p><strong>Conclusion: </strong>Thus, a novel VTX's molecular mechanism in modulating the NLRP3 inflammasome in a time- and area-specific manner in the brain was highlighted, with significant clinical implications in treating depression and cognitive impairments.</p>.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2024-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141616069","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}

{"title":"Myeloid-derived Suppressor Cells and Multiple Sclerosis.","authors":"Aurora Zanghì, Paola Sofia Di Filippo, Carlo Avolio, Emanuele D'Amico","doi":"10.2174/1570159X22999240710142942","DOIUrl":"10.2174/1570159X22999240710142942","url":null,"abstract":"<p><p>Myeloid-Derived Suppressor Cells (MDSCs) are a heterogeneous population of immature myeloid cells that play important roles in maintaining immune homeostasis and regulating immune responses. MDSCs can be divided into two main subsets based on their surface markers and functional properties: granulocytic MDSCs (G-MDSCs) and monocytic MDSCs (M-MDSCs). Recently greatest attention has been paid to innate immunity in Multiple Sclerosis (MS), so the aim of our review is to provide an overview of the main characteristics of MDSCs in MS and its preclinical model by discussing the most recent data available. The immunosuppressive functions of MDSCs can be dysregulated in MS, leading to an exacerbation of the autoimmune response and disease progression. Antigen-specific peptide immunotherapy, which aims to restore tolerance while avoiding the use of non-specific immunosuppressive drugs, is a promising approach for autoimmune diseases, but the cellular mechanisms behind successful therapy remain poorly understood. Therefore, targeting MDSCs could be a promising therapeutic approach for MS. Various strategies for modulating MDSCs have been investigated, including the use of pharmacological agents, biological agents, and adoptive transfer of exogenous MDSCs. However, it remained unclear whether MDSCs display any therapeutic potential in MS and how this therapy could modulate different aspects of the disease. Collectively, all the described studies revealed a pivotal role for MDSCs in the regulation of MS.</p>.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2024-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141579232","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}

{"title":"Ischemic Stroke and Autophagy: The Roles of Long Non-Coding RNAs.","authors":"Longqiang Ouyang, Wenyan Xia, Ameen Abdulhasan Al-Alwany, Reena Gupta, Ibrokhim Sapaev, Sami G Almalki, Saud Almawash, Rand Ali Ziyad, Ahmed Hussien Alawadi, Ali Alsalamy","doi":"10.2174/1570159X22666240704123701","DOIUrl":"https://doi.org/10.2174/1570159X22666240704123701","url":null,"abstract":"<p><p>Ischemic stroke is a significant cause of morbidity and mortality worldwide. Autophagy, a process of intracellular degradation, has been shown to play a crucial role in the pathogenesis of ischemic stroke. Long non-coding RNAs (lncRNAs) have emerged as essential regulators of autophagy in various diseases, including ischemic stroke. Recent studies have identified several lncRNAs that modulate autophagy in ischemic stroke, including MALAT1, MIAT, SNHG12, H19, AC136007. 2, C2dat2, MEG3, KCNQ1OT1, SNHG3, and RMRP. These lncRNAs regulate autophagy by interacting with key proteins involved in the autophagic process, such as Beclin-1, ATG7, and LC3. Understanding the role of lncRNAs in regulating autophagy in ischemic stroke may provide new insights into the pathogenesis of this disease and identify potential therapeutic targets for its treatment.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":null,"pages":null},"PeriodicalIF":4.8,"publicationDate":"2024-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141632942","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}