Frontiers in Cellular Neuroscience最新文献

{"title":"Editorial: Ion channels in the nervous system.","authors":"Janire Urrutia, Alvaro Villarroel, Miren Revuelta","doi":"10.3389/fncel.2026.1812138","DOIUrl":"https://doi.org/10.3389/fncel.2026.1812138","url":null,"abstract":"","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1812138"},"PeriodicalIF":4.0,"publicationDate":"2026-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13035503/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147591014","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":"Establishing an experimental model approach to thermal-induced spinal cord injury in mice.","authors":"Arata Mashima, Kazuya Yokota, Kazu Kobayakawa, Hirokazu Saiwai, Kazuki Kitade, Jun Kishikawa, Mami Sugano, Shintaro Sasaguri, Kiyoshi Tarukado, Kenichi Kawaguchi, Gentaro Ono, Takeshi Maeda, Yasuharu Nakashima","doi":"10.3389/fncel.2026.1779728","DOIUrl":"https://doi.org/10.3389/fncel.2026.1779728","url":null,"abstract":"<p><p>Neurological deficits following spinal surgery represent a severe complication, and thermal damage from high-speed drills is considered a potential cause, but the underlying pathophysiology remains poorly understood. Here, we aimed to develop and characterize a novel mouse model of thermal-induced spinal cord injury (TiSCI). Given that surgical drilling can generate temperatures of 90 °C, we created a TiSCI model by applying a controlled thermal exposure (90 °C for 1 min) to the exposed thoracic cord in mice. The TiSCI model induced significant and persistent hindlimb motor deficits, accompanied by marked demyelination and progressive collagen deposition at the lesion site. Transcriptomic analysis by RNA-sequencing revealed that this pathology was associated with a significant upregulation of pro-fibrotic genes, including Col1a1, Col1a2, Tgfβ1, and Acta2. Using Col1a2-EGFP transgenic mice, we identified a prominent fibrotic scar composed of Type I collagen-producing cells at the lesion site, evident by 7 and 14 days post-injury, which spatially overlapped with demyelinated regions devoid of axons. KEGG pathway analysis highlighted pathways related to extracellular matrix organization, phagocytosis, and fibroblast activation. Notably, Scarb3 and Actg2 were upregulated early, while Itgax and Fzd7 were induced later, implicating both immune cell responses and Wnt/β-catenin signaling in fibrotic scar progression. In conclusion, this study established an experimental platform for investigating TiSCI in mice, providing first direct evidence that a thermal insult causes persistent neurological deficits by inducing a robust fibrotic response. The resulting collagenous scar acts as a physical barrier to axonal connectivity, establishing the fibrotic process as a key therapeutic target.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1779728"},"PeriodicalIF":4.0,"publicationDate":"2026-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13037712/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147591007","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":"Altered lipid peroxidation, perineuronal net and oligodendrocyte markers in the frontal cortex of a dual-hit neurodevelopmental model support its relevance to schizophrenia.","authors":"Victoria Esuaikoh, Sarah Ibegbulam, Alistair Cook, Bianca McFarland, Nora Nunnington, Ambalangoda Perera, Jingjing Feng, Jennifer A Cale, Madeleine V King","doi":"10.3389/fncel.2026.1784522","DOIUrl":"10.3389/fncel.2026.1784522","url":null,"abstract":"<p><strong>Introduction: </strong>The pathogenesis of schizophrenia begins in early neurodevelopment and leads to an array of frontal cortical deficits. They include redox dysregulation, white matter perturbation, loss of perineuronal nets (PNNs) and reduced synaptic density. It is therefore highly desirable that preclinical models used to understand disease, select drug targets and evaluate novel therapeutics encompass similar changes. One approach to improved preclinical modeling incorporates dual-hit neurodevelopmental interventions, like neonatal administration of phencyclidine (PCP, to disrupt development of glutamatergic circuitry) then post-weaning isolation (Iso, to mimic adolescent social stress). We recently showed that rats exposed to PCP-Iso develop GABAergic and inflammatory changes in the frontal cortex, and the current study expands on this by comparing changes to additional cellular and extracellular matrix markers relevant to oxidative stress, myelination, PNN integrity and synaptic vesicle density.</p><p><strong>Methods: </strong>The study used tissue from a previously described cohort of male Lister-hooded rats. They received saline vehicle (Veh, 1 ml/kg s.c.) or PCP (10 mg/kg s.c) on postnatal days (PND) 7, 9 and 11 then were housed in social groups (Gr, 3-4/cage) or post-weaning isolation from PND 21 onwards. Declarative memory was assessed in adulthood (PND 57-80) using a novel object discrimination (NOD) test. Frontal cortical samples were obtained on PND 79-80 and used for immunohistochemical or lectin binding examinations of the lipid peroxidation product 4-hydroxynonenal (4-HNE), oligodendrocyte-associated protein 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase), PNNs and synaptic vesicle glycoprotein 2A (SV2A) throughout the orbitofrontal, prelimbic and infralimbic cortices. In each case data from dual-hit PCP-Iso and single-hit Veh-Iso were compared to each other, and to data from Veh-Gr controls.</p><p><strong>Results: </strong>Single-hit isolation-reared and dual-hit PCP-Iso both showed impaired declarative memory. They also both exhibited reduced PNN density in the orbitofrontal cortex and reduced PNN thickness in the prelimbic/infralimbic cortex. However, PCP-Iso showed additional PNN thinning, 4-HNE upregulation and CNPase downregulation in orbitofrontal regions.</p><p><strong>Discussion: </strong>These findings enhance the face validity of PCP-Iso and support wider use of this preclinical model for evaluating novel therapeutics designed to support parvalbumin-positive neurons and PNNs, promote myelination or normalize redox dysregulation. Unaltered SV2A expression in young adult PCP-Iso mirrors recent dorsolateral prefrontal cortical findings in first-episode psychosis, supports expectations that increased microglial activation precedes aberrant synaptic pruning, and justifies further examinations of synaptic markers in PCP-Iso at later developmental stages.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1784522"},"PeriodicalIF":4.0,"publicationDate":"2026-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13033504/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147591090","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":"Glial D-serine modulates oligodendrocyte lineage progression under inflammatory conditions.","authors":"Juan Pablo Espinoza, Ignacio Cisterna, Juan Jose Triviño, Verónica Arancibia, Sebastián Beltrán-Castillo","doi":"10.3389/fncel.2026.1784678","DOIUrl":"10.3389/fncel.2026.1784678","url":null,"abstract":"<p><p>Inflammatory environments may shape oligodendrocyte lineage dynamics beyond classical cytokine signaling, in part through the release of glial neuromodulators. Here, we investigated whether inflammation-associated D-serine signaling modulates oligodendrocyte lineage progression. Using highly purified primary oligodendrocyte precursor cell (OPC) cultures, we show that D-serine exposure during late differentiation reduces the proportion of OLIG2⁺ and myelin basic protein-positive (MBP⁺) cells without altering net cell number, while selectively decreasing apoptosis within the mature MBP⁺ population. These findings indicate that D-serine attenuates late-stage lineage progression while preserving oligodendrocyte survival <i>in vitro</i>. In parallel, inflammatory activation of mixed glial cultures with lipopolysaccharide (LPS) increased tumor necrosis factor-<i>α</i> release, upregulated serine racemase expression, and elevated extracellular D-serine levels. Conditioned media from reactive glial cultures recapitulated the effects of D-serine on OPC maturation, which were prevented by enzymatic degradation of D-serine or pharmacological blockade of N-methyl-D-aspartate receptors (NMDARs). Together, these findings support the involvement of glia-derived D-serine as a modulatory signal influencing oligodendrocyte lineage progression consistent with NMDAR-dependent mechanisms under inflammatory conditions that may contribute to impaired remyelination.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1784678"},"PeriodicalIF":4.0,"publicationDate":"2026-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13033550/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147591058","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":"Correction: Advances in astrocytic calcium signaling research.","authors":"Yuzhu Chen, Yejun Ye, Joyce Jia, Binhao Long, Tingting Dou, Xingke Yan","doi":"10.3389/fncel.2026.1821571","DOIUrl":"10.3389/fncel.2026.1821571","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.3389/fncel.2025.1719532.].</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1821571"},"PeriodicalIF":4.0,"publicationDate":"2026-03-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13034784/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147591072","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":"Neurovascular dysfunction in the development and progression of neuroinflammatory diseases.","authors":"Jamila Gowdy, Julie Ahn, Robert H Miller, Yusra Islam","doi":"10.3389/fncel.2026.1741928","DOIUrl":"10.3389/fncel.2026.1741928","url":null,"abstract":"<p><p>The neurovascular unit (NVU) is critical for brain homeostasis through its roles in maintenance of an effective blood brain barrier (BBB) and regulation of cerebral blood flow. Perturbation of the NVU is a hallmark of the pathology of multiple neurodegenerative diseases resulting in loss of BBB integrity, neuroinflammation and neuronal dysfunction. The NVU is a complex structure composed of endothelial cells, pericytes, as well as central nervous system (CNS) glial and neuronal components. While the importance of the CNS vasculature in health and disease is well established, the mechanisms underlying vascular pathology and its contributions to neurodegenerative diseases are less well defined. Neuroinflammation and reactive gliosis occurs in the majority of neurodegenerative diseases and recent studies suggest that immune mediated disruption of the BBB contributes to the induction of reactive gliosis and neuronal dysfunction. Potential consequences of NVU disruption include immune-driven vascular inflammation and leukocyte infiltration in Multiple Sclerosis (MS), protease-mediated tight junction degradation in ischemic stroke (IS), <i>α</i>-synuclein-associated endothelial dysfunction in Parkinson's Disease (PD), amyloid-<i>β</i>- and tau-induced pericyte injury in Alzheimer's Disease (AD), and complement-mediated vascular damage in Amyotrophic Lateral Sclerosis (ALS). Here we review the nature of NVU perturbations in these common neurodegenerative diseases, with an emphasis on the contribution of immune modulation of BBB disruption in neuropathology and disease progression.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1741928"},"PeriodicalIF":4.0,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13021429/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147573045","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":"Function of the large intestine and its interaction with the brain after ischemic stroke: a comprehensive literature review.","authors":"Xuan Jia, Leticia Simo, Sydni Rosenfeld, Fengwu Li, Yingnan Zhou, Yuchuan Ding, Xiaokun Geng","doi":"10.3389/fncel.2026.1735569","DOIUrl":"10.3389/fncel.2026.1735569","url":null,"abstract":"<p><p>The large intestine, part of the distal gastrointestinal tract, is vital for water and electrolyte absorption and microbial fermentation. It is also a significant immune organ endowed with an extensive and intricate neural network. Intestinal epithelial cells are essential for endocrine regulation and maintaining the integrity of the intestinal barrier. Stroke, a leading cause of adult mortality and disability, occurs when there is a lack of oxygen to the brain and involves complex cerebrovascular dynamics that significantly impact systemic functions. In this framework, the gut-brain axis-the bidirectional circuitry connecting the gut and the central nervous system (CNS)-emerges as a critical interface. This review examines the immunological, neurological, endocrine, and barrier functions of the large intestine and explores its interplay with stroke pathophysiology. By detailing the interrelation between stroke and large intestinal functions, this paper aims to provide a foundational reference for advancing research into their intertwined mechanisms and identifying potential therapeutic targets.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1735569"},"PeriodicalIF":4.0,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13017306/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147573021","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":"Silencing MALAT1 represses pathological progression, inflammation, and vascular smooth muscle cell phenotype switching by regulating the SEMA3C-mediated Smad pathway in intracranial aneurysms.","authors":"Junlong Kang, Wei Li, Xinjie Gao, Xinhua Tian, Wei Feng, Xiang Yao, Feng Wei, Luyue Chen, Hongjin Chen, Junjiang Tong, E Chen, Yuxiang Gu","doi":"10.3389/fncel.2026.1706518","DOIUrl":"10.3389/fncel.2026.1706518","url":null,"abstract":"<p><strong>Background: </strong>The crucial role of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in regulating aneurysm formation, inflammation, and neural dysfunction has gradually been recognized. This study aimed to evaluate the effects of MALAT1 modification on pathological changes, inflammation, vascular smooth muscle cell (VSMC) phenotype switching, and the underlying mechanism in intracranial aneurysms (IAs).</p><p><strong>Methods: </strong>MALAT1-overexpressing (oeMALAT1), MALAT1 short hairpin (shMALAT1), and semaphorin 3C (SEMA3C)-overexpressing (oeSEMA3C) lentiviruses were transfected alone or in combination into basilar artery VSMCs originating from IA rats. These lentiviruses were then stereotactically injected into IA rats.</p><p><strong>Results: </strong><i>In vitro</i>, the overexpression of MALAT1 inhibited cell proliferation while promoting cell apoptosis and invasion; the release of TNF-α, IL-1β, and IL-6; and the transformation of IA basilar artery VSMCs from the contractile type to the synthetic type. However, the silencing of MALAT1 had the opposite effect. The silencing of MALAT1 downregulated SEMA3C, and its silencing inactivated the Smad pathway. Furthermore, SEMA3C overexpression attenuated the effects of MALAT1 silencing on IA basilar artery VSMC proliferation, apoptosis, invasiveness, proinflammatory cytokines, phenotype switching, and Smad pathway inactivation. <i>In vivo</i>, silencing MALAT1 reduced the release of TNF-α, IL-1β, and IL-6, decreased pathological progression, inhibited VSMC synthetic type switching, and inactivated the Smad pathway in IA rats. However, the overexpression of SEMA3C reversed these effects.</p><p><strong>Conclusion: </strong>Silencing MALAT1 represses pathological progression, inflammation, and VSMC phenotype switching by regulating the SEMA3C-mediated Smad pathway in IA.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1706518"},"PeriodicalIF":4.0,"publicationDate":"2026-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13013063/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147520550","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":"Reduced peripheral serotonin levels in women with multiple sclerosis: associations with underweight status, treatment duration, and use of interferon beta 1a.","authors":"Gilberto Pérez-Sánchez, León Arturo Aguilar-Gómez, Giselle Berenice Vela-Sancho, Salomón Jacinto-Gutiérrez, Enrique Becerril-Villanueva, Samantha Alvarez-Herrera, Luis Vallejo-Castillo, María Paulina Reyes-Mata, Mario Alberto Mireles-Ramírez, José de Jesús Guerrero-García, Daniel Ortuño-Sahagún, Lenin Pavón","doi":"10.3389/fncel.2026.1752975","DOIUrl":"10.3389/fncel.2026.1752975","url":null,"abstract":"<p><p>Multiple sclerosis (MS) is a chronic autoimmune-mediated demyelinating disease of the CNS, characterized by neuroinflammatory, axonal degeneration, and pronounced sexual dimorphism. Experimental data implicate dysregulated 5-HT levels in MS. However, the effects of clinical parameters and disease-modifying-therapies (DMTs) on peripheral 5-HT concentrations remain underexplored. This study aimed to quantify peripheral levels of tryptophan (Trp), 5-HT, and 5-hydroxyindoleacetic acid (5-HIAA) in patients with relapsing-remitting MS (RRMS) and to assess the effects of BMI, DMT duration, and specific DMT regimens. In this cross-sectional analysis, 226 participants were enrolled and stratified into four groups: healthy men (HM; <i>n</i> = 29), healthy women (HW; <i>n</i> = 84), men with RRMS (MMS; <i>n</i> = 29), and women with RRMS (WMS; <i>n</i> = 84). Serum concentrations of Trp, 5-HT, and 5-HIAA were measured using reverse-phase high-performance liquid chromatography (HPLC) with fluorescence detection. Nonparametric statistical tests were applied. Peripheral 5-HT levels were significantly reduced in underweight WMS (BMI < 18 kg/m²; <i>p</i> < 0.05), WMS with DMT duration over 4 years (<i>p</i> < 0.01), and WMS receiving interferon beta-1a (<i>p</i> < 0.01) compared to HW. No significant intergroup differences in Trp or 5-HIAA were observed across all stratifications. These findings reveal a novel association between reduced peripheral 5-HT and specific clinical-therapeutic factors in WMS, extending recent MS research on sex-specific vulnerabilities, serotonergic dysregulation in neuroinflammation, and psychiatric comorbidity. By highlighting the influence of low BMI, prolonged DMT exposure, and interferon beta-1a on 5-HT homeostasis, this study underscores the need for multidisciplinary management integrating neurological and psychiatric care in WMS and suggests avenues for precision interventions targeting serotonergic pathways to reduce disease burden.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1752975"},"PeriodicalIF":4.0,"publicationDate":"2026-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13013054/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147520590","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":"Preclinical models of stem cell-mediated analgesia and tissue repair: mechanisms, challenges, and future directions.","authors":"Minshun Zhu, Hao Zhang, Long Liang, Sanbing Wu, Jiaping Chen","doi":"10.3389/fncel.2026.1787909","DOIUrl":"10.3389/fncel.2026.1787909","url":null,"abstract":"<p><p>As an emerging biological therapeutic approach, stem cell therapy demonstrates broad application prospects in analgesia and tissue regeneration, particularly achieving significant advances in treating conditions such as spinal cord injury and intervertebral disc degeneration. In recent years, preclinical model studies have deepened our understanding of the mechanisms underlying stem cell-mediated pain relief and tissue repair, revealing their potential to regulate inflammatory responses, promote nerve regeneration, and repair damaged tissues through multiple pathways. However, the heterogeneity of preclinical models and the discrepancies between these models and clinical practice, coupled with often insufficient critical appraisal of study quality, remain critical issues requiring urgent resolution in this field. This narrative review systematically summarizes the fundamental theories and key mechanisms underlying stem cell-mediated analgesia and regeneration. It comprehensively evaluates the advantages and limitations of different animal models, critically analyzes major controversies and technical challenges in research, and identifies key directions for future studies. The literature discussed herein was identified through searches in PubMed and Web of Science databases, focusing on recent preclinical studies (primarily within the last decade) involving stem cells, pain models, and tissue regeneration. Selected studies were evaluated for their methodological rigor and contribution to mechanistic understanding. This review aims to synthesize current evidence, critically appraise preclinical models, and provide a forward-looking perspective for research on stem cell-related analgesia and regenerative mechanisms, thereby promoting further development in clinical translation.</p>","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":"20 ","pages":"1787909"},"PeriodicalIF":4.0,"publicationDate":"2026-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13012907/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147520574","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}