Frontiers in Cellular Neuroscience最新文献

{"title":"Broccoli for the brain: a review of the neuroprotective mechanisms of sulforaphane.","authors":"Riley N Bessetti, Karen A Litwa","doi":"10.3389/fncel.2025.1601366","DOIUrl":"10.3389/fncel.2025.1601366","url":null,"abstract":"<p><p>Sulforaphane, a phytochemical abundant in the sprouts of cruciferous vegetables, protects plants during a critical period of development. Through sulforaphane's ability to activate the mammalian Nuclear Factor Erythroid 2-related Factor 2 (NRF2) pathway, these beneficial properties extend beyond plants. Our current review explores emerging neuroprotective mechanisms of sulforaphane and their relation to neurological disorders. Primarily, we discuss the ability of sulforaphane to mitigate oxidative stress and prevent neuroinflammation. Given sulforaphane's ability to activate multiple cytoprotective mechanisms, sulforaphane is emerging as a promising therapeutic for multiple neurodegenerative and neurodevelopmental disorders. In this review, we highlight current clinical trials in neurological disorders and conclude by discussing therapeutic opportunities and challenges for sulforaphane. Together, preclinical models and clinical trials highlight emerging themes of sulforaphane-mediated neuroprotection, including hormetic responses that depend upon the cell/tissue, neurological condition, insult, and developmental stage. In particular, low sulforaphane doses consistently exhibit beneficial effects in preclinical neuronal cell cultures models and avoid cytotoxic effects of higher sulforaphane doses. These factors will be important considerations in informing therapeutic use of sulforaphane.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1601366"},"PeriodicalIF":4.2,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12271217/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144674238","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}

{"title":"Chronic benzodiazepine treatment triggers gephyrin scaffold destabilization and GABA_AR subsynaptic reorganization.","authors":"Caitlyn A Chapman, Nadya Povysheva, Tyler B Tarr, Jessica L Nuwer, Stephen D Meriney, Jon W Johnson, Tija C Jacob","doi":"10.3389/fncel.2025.1624813","DOIUrl":"https://doi.org/10.3389/fncel.2025.1624813","url":null,"abstract":"<p><p>Benzodiazepines (BZDs) are important clinical drugs with anxiolytic, anticonvulsant, and sedative effects mediated by potentiation of inhibitory GABA type A receptors (GABA_ARs). Tolerance limits the clinical utility of BZDs, yet the mechanisms underlying tolerance after chronic exposure have not been thoroughly investigated. Here, we assessed the impact of chronic (7-day) treatment with the BZD diazepam (DZP) on the dynamic plasticity and subsynaptic organization of the gephyrin scaffold and γ2 subunit-containing GABA_ARs in primary neurons. After functional confirmation of diminished BZD sensitivity, we provide the first super-resolution analysis of inhibitory nanoscale plasticity induced by chronic BZD exposure: gephyrin subsynaptic domains were smaller and the inhibitory postsynaptic area was overall diminished by DZP treatment, resulting in a condensation of synaptic γ2-GABA_ARs into smaller synaptic areas. Using a novel fluorescence-based <i>in situ</i> proximity ligation assay and biochemical fractionation analysis, the mechanism for gephyrin downregulation was revealed to be dependent on phosphorylation and protease cleavage. Accordingly, DZP treatment impaired gephyrin synaptic stability, demonstrated by live-imaging photobleaching experiments. Despite the loss of BZD sensitivity and stable synaptic gephyrin, 7-day DZP treatment did not reduce the surface or total protein levels of BZD-sensitive γ2-GABA_ARs, as shown in prior short-term BZD treatment studies. Instead, chronic DZP treatment induced an accumulation of γ2-GABA_ARs in the extrasynaptic membrane. Surprisingly, γ2-GABA_AR interactions with gephyrin were also enriched extrasynaptically. An identified rise in extrasynaptically-localized gephyrin cleavage fragments may function to confine receptors away from the synapse, as supported by a decrease in extrasynaptic γ2-GABA_AR mobility. Altogether, we find that chronic BZD treatment triggers several subtle converging plasticity events at inhibitory synapses which effectively restrict the synaptic renewal of BZD-sensitive GABA_ARs via mechanisms distinct from those observed with short-term treatment.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1624813"},"PeriodicalIF":4.2,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12271172/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144674239","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}

{"title":"Tear deficiency transforms spatial distribution of corneal calcitonin gene-related peptide-positive nerves in rats.","authors":"Takeshi Kiyoi, Akihiro Nakajima, Qiang He, Li Liu, Shijie Zheng, Shizuka Kobayashi, Junsuke Uwada, Takayoshi Masuoka","doi":"10.3389/fncel.2025.1619310","DOIUrl":"10.3389/fncel.2025.1619310","url":null,"abstract":"<p><p>The nerve terminals distributed in the cornea are important for sensory perception and the maintenance of ocular surface homeostasis. In dry eye disease (DED), corneal nerves undergo functional and morphological changes that may be involved in abnormal ocular surface sensation and corneal pathology. However, changes in the spatial distribution of corneal nerves, including polymodal nociceptors, and their regulatory mechanisms remain unknown. In the present study, we analyzed time-dependent changes in corneal nerves, focusing on calcitonin gene-related peptide (CGRP)-positive nociceptive nerves in DED model rats, in which both the extraorbital and intraorbital lacrimal glands were surgically excised. After gland excision, the cornea showed acute inflammation, characterized by the presence of segmented-nucleus neutrophil infiltration, followed by chronic inflammation and angiogenesis. In parallel, denervation and subsequent reinnervation in the epithelium, as well as excessive innervation in the stroma, were observed, both involving CGRP-positive nerves. The DED rats showed hypoesthesia and subsequently hyperesthesia in response to mechanical stimulation of the corneal surface, which was synchronized with the denervation and reinnervation of corneal nerve plexuses in the epithelium. Persistent hyperalgesia to capsaicin in DED rats was not correlated with CGRP-positive nerve distribution in the early phase. After gland excision, the expression of neurotropic factor Sema7A increased within the epithelium and stroma, while that of the repulsive axon guidance factor Sema3A decreased in the epithelium. The expression patterns of these molecules correlate with reinnervation of the epithelium and excessive innervation of the stroma. These data suggest that changes in nerve distribution, including CGRP-positive nerves, might partially contribute to sensory perception and progression of corneal inflammatory pathology in DED. Sema3A and Sema7A may be involved in reinnervation as part of the regulatory mechanism in DED.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1619310"},"PeriodicalIF":4.2,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12259659/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144642209","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}

{"title":"Potassium channel clustering: mechanisms shaping axonal excitability.","authors":"Gabriel Escobedo, Matthew N Rasband","doi":"10.3389/fncel.2025.1627517","DOIUrl":"10.3389/fncel.2025.1627517","url":null,"abstract":"<p><p>The precise clustering of ion channels at axon initial segments (AIS) and nodes of Ranvier is essential for axonal excitability and rapid action potential propagation. Among the axonal ion channels, voltage-gated potassium channels (Kv) and two-pore domain potassium (K2P) leak channels are key regulators of AIS and nodal excitability. Kv7 and Kv1 channels contribute to action potential threshold and repolarization at the AIS, and membrane repolarization in axons has historically been attributed to Kv channels. However, recent studies suggest that at nodes of Ranvier K2P channels, particularly TRAAK and TREK-1, play a dominant role in action potential repolarization. The interaction of Kv and K2P channels with diverse scaffolding proteins ensures their precise localization at AIS and nodes. Mislocalization or dysfunction of axonal Kv and K2P channels can cause epilepsy and neurodevelopmental disorders. This review explores the diversity of potassium channels and the mechanisms responsible for their clustering at AIS and nodes of Ranvier. Understanding these processes will be essential for therapeutic strategies aimed at treating diseases characterized by abnormal potassium channel expression, clustering, and function in neurons.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1627517"},"PeriodicalIF":4.2,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12259577/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144642208","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}

{"title":"Circulating exosomes with unique lipid signature in relapsing remitting multiple sclerosis.","authors":"Claudia Palazzo, Ilaria Asci, Silvia Russo, Cinzia Buccoliero, Vincenzo Mangialardi, Pasqua Abbrescia, Onofrio Valente, Maddalena Ruggieri, Damiano Paolicelli, Simona Lobasso, Antonio Frigeri","doi":"10.3389/fncel.2025.1613618","DOIUrl":"10.3389/fncel.2025.1613618","url":null,"abstract":"<p><p>Exosomes are small, membrane-bound vesicles secreted by most cell types into the extracellular environment. They play a crucial role in intercellular communication by transporting bioactive molecules, including proteins, lipids, and RNAs, thereby influencing the phenotype and potentially the genotype in recipient cells. In recent years, exosomes have gained increasing attention in the study of pathophysiological conditions and numerous diseases, including multiple sclerosis (MS), an autoimmune disorder with myelin sheath and neuroaxonal damage in the central nervous system. In this study, we isolated and purified serum-derived exosomes from patients with relapsing remitting MS (RR-MS) and characterized their lipid profiles using matrix-assisted laser desorption ionization-time-of-flight/mass spectrometry (MALDI-TOF/MS). Lipid analysis was performed in both negative and positive ion modes on intact exosomes, bypassing lipid extraction steps and significantly reducing sample-processing time. The lipid profiles of RR-MS exosomes were compared to those of exosomes isolated from the serum of healthy subjects (HS), and statistical analysis was applied to mass spectra to identify potential lipid biomarkers. The specific phospholipid marker of exosomal membranes, bis(monoacylglycero)phosphate (BMP), was clearly detected in both MALDI lipid profiles, with no significant differences in its content between the two sample groups. However, RR-MS exosomes exhibited significantly lower levels of phosphatidic acid (PA) compared to HS exosomes, despite PA being a key structural component of extracellular vesicles. Notably, comparative analysis revealed an enrichment of several lysophosphatidylcholine (LPC) species in RR-MS exosome membranes, aligning with their known proinflammatory role in MS pathology. Our most significant finding was a markedly lower phosphatidylcholine (PC) to LPC ratio in the pathological group indicating potential alterations in membrane lipid homeostasis. To the best of our knowledge, this study is the first to report a distinct lipid signature in serum-derived exosomes from RR-MS patients using direct MALDI-TOF/MS analysis.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1613618"},"PeriodicalIF":4.2,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12245768/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625749","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}

{"title":"Sialylation as a checkpoint for inflammatory and complement-related retinal diseases.","authors":"Yiduo Min, German Cuevas-Rios, Thomas Langmann, Harald Neumann","doi":"10.3389/fncel.2025.1623755","DOIUrl":"10.3389/fncel.2025.1623755","url":null,"abstract":"<p><p>Sialylation is a modification process involving the addition of sialic acid residues to the termini of glycoproteins and glycolipids in mammalian cells. Sialylation serves as a crucial checkpoint inhibitor of the complement and immune systems, particularly within the central nervous system (CNS), including the retina. Complement factor H (FH), complement factor properdin (FP), and sialic acid-binding immunoglobulin-like lectin (SIGLEC) receptors of retinal mononuclear phagocytes are key players in regulating the complement and innate immune systems in the retina by recognizing sialic acid (Sia) residues. Intact retinal sialylation prevents any long-lasting and excessive complement or immune activation in the retina. However, sialylated glycolipids are reduced in the CNS with aging, potentially contributing to chronic inflammatory processes in the retina. Particularly, genetically induced hyposialylation in mice leads to age-related, complement factor C3-mediated retinal inflammation and bipolar cell loss. Notably, most of the gene transcript pathways enriched in the mouse retina, following genetically induced hyposialylation, are also involved in age-related macular degeneration (AMD). Interestingly, intravitreal application of polysialic acid (polySia) controlled the innate immune responses in the mouse retina by blocking mononuclear phagocyte reactivity, inhibiting complement activation, and protecting against vascular damage in two different humanized SIGLEC-11 animal models. Accordingly, a polySia polymer conjugate has entered clinical phase II/III testing in patients with geographic atrophy secondary to AMD. Thus, hyposialylation or dysfunctional sialylation should be considered as an age-related contributor to inflammatory retinal diseases, such as AMD. Consequently, sialic acid-based biologics could provide novel therapies for complement-related retinal diseases.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1623755"},"PeriodicalIF":4.2,"publicationDate":"2025-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12245909/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625750","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}

{"title":"PTEN in somatostatin neurons regulates fear and anxiety and is required for inhibitory synaptic connectivity within central amygdala.","authors":"Timothy W Holford, Kaitlyn N Letourneau, Carolyn Von-Walter, Daniela Moncaleano, Cody L Loomis, M McLean Bolton","doi":"10.3389/fncel.2025.1597131","DOIUrl":"10.3389/fncel.2025.1597131","url":null,"abstract":"<p><strong>Introduction: </strong>The phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is a negative regulator of the mTOR pathway and is strongly associated with autism spectrum disorder (ASD), with up to 25% of ASD patients with macrocephaly harboring PTEN mutations. Mice with germline PTEN haploinsufficiency show behavioral characteristics resembling ASD, as do various mouse models with conditional knockouts of PTEN. Human tissue studies and those from multiple genetic mouse models suggest that dysfunction of GABAergic interneurons may play a role in the development of ASD, but the precise mechanisms remain elusive. PTEN provides a target for investigation because it regulates the development of inhibitory neurons arising from the medial ganglionic eminence, promoting the survival and maturation of parvalbumin (PV+) neurons at the expense of somatostatin (SOM+) neurons.</p><p><strong>Methods: </strong>Here, we investigate how PTEN regulates SOM+ neurons at the cellular and circuit level in the central lateral amygdala (CeL), an area that governs the key ASD behavioral symptoms of social anxiety and altered emotional motivation for social engagement using behavioral analysis, electrophysiology, and two-photon local circuit mapping.</p><p><strong>Results: </strong>We found that knocking out PTEN in SOM+ neurons results in elevated levels of fear and anxiety and decreases CeL local circuit connectivity. Specifically, this manipulation decreased the strength of connections between individual neurons and altered the distribution of local connections in a cell-type specific manner. In contrast to the deficit in local inhibitory connections within CeL, the excitatory drive from the major CeL input, the basolateral amygdala (BLA) was enhanced.</p><p><strong>Discussion: </strong>This combined imbalance of enhanced excitation and diminished local inhibition likely underlies the heightened fear learning and anxiety we observed in the PTEN-SOM-KO mice.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1597131"},"PeriodicalIF":4.2,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12240933/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144607921","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}

{"title":"Is environmental enrichment effective in modulating autophagy markers in the brain exposed to adverse conditions? A systematic review.","authors":"Clarice Beatriz Gonçalves Silva, Matheus Santos de Sousa Fernandes, Debora Dantas Nucci Cerqueira, Gabriela Carvalho Jurema Santos, Fatma Hilal Yagin, Yalin Aygun, Georgian Badicu, Fabiana S Evangelista, Pablo Prieto-González, Fabrício Oliveira Souto, Ashit Kumar Dutta, Sameer Badri Al-Mhanna, Abedelmalek Kalefh Tabnjh","doi":"10.3389/fncel.2025.1624500","DOIUrl":"10.3389/fncel.2025.1624500","url":null,"abstract":"<p><p>Autophagy is a key regulator of cellular homeostasis and neuronal survival, particularly under adverse physiological conditions. Environmental enrichment (EE), a non-pharmacological intervention providing enhanced sensory, cognitive, and motor stimulation, may modulate autophagic processes in the brain. This systematic review aimed to synthesize preclinical findings on the effects of EE on autophagy markers in rodent models subjected to diverse adverse conditions. A literature search across PubMed, Scopus, ScienceDirect, and embase yielded eight eligible studies meeting inclusion criteria. EE was found to be generally associated with upregulation of key autophagic markers such as Beclin-1, LC3-II/LC3-I ratio, cathepsins, p62, p-TFEB, and LAMP-1 across brain regions including the cortex, hippocampus, and penumbral area. However, reductions in some markers were also observed, indicating that the modulatory effects of EE are context-dependent and may vary with disease model, brain region, or EE protocol duration. These findings suggest that EE holds promise as an adjunctive strategy to modulate autophagy and mitigate neurodegeneration, though heterogeneity in study design and outcomes warrants caution during interpretation. Further mechanistic and sex-specific studies are needed to clarify the therapeutic relevance of EE-induced autophagic modulation.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1624500"},"PeriodicalIF":4.2,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12238764/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144599915","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}

{"title":"The role of oxidative stress in spinal cord ischemia reperfusion injury: mechanisms and therapeutic implications.","authors":"Yu Xing, Yuan-Zhang Xiao, Min Zhao, Jiang-Jun Zhou, Kai Zhao, Chun-Lin Xiao","doi":"10.3389/fncel.2025.1590493","DOIUrl":"10.3389/fncel.2025.1590493","url":null,"abstract":"<p><p>Spinal cord ischemia/reperfusion injury (SCIRI) is a serious disease that leads to the loss of sensory and motor functions and is a common complication after spinal cord injury, spinal cord degeneration or thoracic and abdominal aortic surgery. At present, the spinal cord is mainly protected from ischemic injury through treatment strategies such as hypothermia, surgery and drug assistance, but these intervention measures cannot effectively improve these conditions. SCIRI is a complex process that leads to cell damage and death. Among them, oxidative stress is an important pathological event of ischemia/reperfusion injury. Oxidative stress can initiate multiple inflammatory and apoptotic pathways, triggering a series of destructive events such as inflammatory responses and cell death, further deteriorating the microenvironment at the injured site, and leading to neurological dysfunction. Based on the important role of oxidative stress in SCIRI, we believe that targeted inhibition of oxidative stress responses can effectively reduce secondary injuries caused by trauma, which has a certain positive effect on the rehabilitation and prognosis of patients with SCIRI. This review systematically expounds the spatiotemporal dynamic characteristics of oxidative stress during the SCIRI process and its molecular regulatory network, with a focus on analyzing the multivariate generation mechanism of ROS. To deeply explore the regulatory effects of ROS on pathological processes such as neuronal death, inflammatory response and blood-spinal barrier disruption under SCIRI conditions, as well as its interaction patterns with signaling pathways. In order to form a systematic treatment for SCIRI caused by oxidative stress and promote the recovery of neurological function after injury. This review is helpful for us to understand the effect of oxidative stress on SCIRI and provides a theoretical basis for the treatment of SCIRI based on oxidative stress.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1590493"},"PeriodicalIF":4.2,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12236186/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144590843","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}

{"title":"Corrigendum: <i>O</i> ⁶-methylguanine DNA methyltransferase (MGMT) expression in U1242 glioblastoma cells enhances <i>in vitro</i> clonogenicity, tumor implantation <i>in vivo</i>, and <i>sensitivity</i> to alisertib-carboplatin combination treatment.","authors":"Müge Sak, Brian J Williams, Andrew J Hey, Mayur Sharma, Leslie Schier, Megan J Wilson, Mahatma Ortega, Alyssa I Lara, Mikaela N Brentlinger, Norman L Lehman","doi":"10.3389/fncel.2025.1637837","DOIUrl":"10.3389/fncel.2025.1637837","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.3389/fncel.2025.1552015.].</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"19 ","pages":"1637837"},"PeriodicalIF":4.2,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12235744/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144590842","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}