Molecular Neurobiology最新文献

{"title":"miR-758-3p Interferes with Neuronal Apoptosis in Cerebral Ischemia-Reperfusion by Inhibiting ILK.","authors":"Xiaoli Min, Xuesong Bai, Qing Zhao, Wenwu Yang, Sixian Lin, Lei Xian, Rui Jing, Xuhui Li, Wenji Jia, Wei Miao, Mei Yin, Feifei Shang, Yong Zeng","doi":"10.1007/s12035-025-04736-5","DOIUrl":"10.1007/s12035-025-04736-5","url":null,"abstract":"<p><p>This study investigated the role of integrin-linked kinase (ILK) in neuronal apoptosis induced by cerebral ischemia‒reperfusion injury (CIRI) and its interaction with a circRNA (0000964) and miR-758-3p. Using in vivo and in vitro rat models, we clarified how ILK regulates neuronal apoptosis during CIRI. Our findings revealed that ILK expression is upregulated in response to CIRI and is modulated by the circRNA (0000964)/miR-758-3p axis. This study provides new insights into the molecular mechanisms of CIRI and suggests potential therapeutic targets to reduce neuronal apoptosis. A CIRI rat model was created through middle cerebral artery occlusion (MCAO). After miR-758-3p overexpression, neurological deficits, CIRI volume, and the expression levels of circRNAs (0000964) and ILK were evaluated. Neurons were subjected to oxygen‒glucose deprivation (OGD) to simulate in vitro CIRI, and the same molecules were analyzed. MCAO-induced CIRI downregulated a circRNA (0000964) and upregulated ILK and miR-758-3p. Similarly, in vitro OGD-induced apoptosis downregulated a circRNA (0000964) and upregulated ILK and miR-758-3p. Further analysis confirmed that a circRNA (0000964) negatively regulates miR-758-3p, which in turn negatively regulates ILK. This axis controls ILK and Caspase-3 expression, influencing neuronal apoptosis. ILK has been identified as a key regulator of neuronal apoptosis in CIRI. The circRNA (0000964)/miR-758-3p axis modulates ILK, impacting neuronal survival. This molecular network offers new insights into CIRI pathophysiology and highlights possible therapeutic approaches.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"7805-7819"},"PeriodicalIF":4.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12078447/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143399533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mito-Apocynin Protects Against Kainic Acid-Induced Excitotoxicity by Ameliorating Mitochondrial Impairment.","authors":"Miaomiao Lin, Huanchen Wu, Xiaorui Wan, Na Liu, Yiyue Jiang, Yichao Sheng, Jing Wang, Haidong Xu, Jie Xue, Zhenghong Qin, Yan Wang","doi":"10.1007/s12035-025-04827-3","DOIUrl":"10.1007/s12035-025-04827-3","url":null,"abstract":"<p><p>Neurodegenerative diseases represent significant global health challenges, with rising incidence rates. A substantial body of evidence indicates that excitotoxicity may be a critical target in the context of these diseases. However, effective pharmacological interventions aimed at mitigating excitotoxicity remain elusive. This study aimed to elucidate the neuroprotective effects and mechanisms of the mitochondrion-targeted NOX inhibitor, mito-apocynin, in the context of kainic acid (KA)-induced excitotoxicity. Our findings demonstrate that KA disrupts mitochondrial morphology, leading to impaired energy metabolism and mitochondrial dysfunction. Western blotting experiments revealed that KA compromises mitochondrial quality control. Additionally, Nissl staining and CCK8 assays indicated that mito-apocynin (administered at 75 μg/kg in vivo and 1 μM in vitro) significantly reduced neuronal death resulting from KA-induced excitotoxic damage in both in vivo and in vitro models. Furthermore, mito-apocynin improved neurobehavioral deficits induced by KA and mitigated mitochondrial dysfunction observed in vitro. Notably, mito-apocynin significantly reversed the KA-induced increase in NOX4 levels within the striatal mitochondria, reduced the ratio of phosphorylated DRP1 (Ser616) to total DRP1, and enhanced the expression of PGC-1α, PINK1, and Parkin proteins throughout the total striatum. In summary, mito-apocynin alleviates oxidative stress, preserves normal mitochondrial function and energy metabolism, and promotes mitochondrial quality control by modulating NOX expression in mitochondria, thereby reducing KA-induced excitotoxic damage.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"7160-7173"},"PeriodicalIF":4.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12078395/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143649618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combining Single-Cell RNA Sequencing and Mendelian Randomization to Explore Novel Drug Targets for Parkinson's Disease.","authors":"Xiaolong Wu, Kailiang Wang, Qinghua Li, Yuqing Zhang, Penghu Wei, Yongzhi Shan, Guoguang Zhao","doi":"10.1007/s12035-025-04700-3","DOIUrl":"10.1007/s12035-025-04700-3","url":null,"abstract":"<p><p>Neuroinflammation is a key pathological factor of PD, and T cells play a central role in neuroinflammatory progression. However, the causal effect of T cell-related genes on the risk of PD is still unclear. We explored single-cell RNA sequencing (scRNA-Seq) datasets of the peripheral blood T cells of PD patients and healthy controls, and screened the differentially expressed genes (DEGs) in the cytotoxic CD4 + T cells relative to the other T cell subsets. Pseudo-time series analysis, cell-cell communication analysis, and metabolic pathway analysis was performed for the cytotoxic CD4 + T cells. The DEGs were also functionally annotated through GO and KEGG pathway enrichment analyses. The MR approach was used to establish causal effects of the DEGs (exposure) on PD risk (outcome), and explore new drug targets for PD. The findings of MR analysis were further validated by Steiger filtering, bidirectional MR, Bayesian colocalization analysis, and phenotype scanning, and the GWAS data from an independent PD case-control cohort was used for external validation of the results. Finally, differences in gene expression between PD patients and healthy controls were further validated in scRNA-Seq and bulk transcriptome sequencing data. We found that increased expression of IL-32, GNLY, MT2A, and ARPC2 was significantly associated with a higher risk of PD. In contrast, the increase in ARRB2 was closely related to a lower risk of PD. IL32, GNLY, MT2A, ARRB2, and ARPC2 are the causal genes and potential drug targets of PD. Cytotoxic CD4 + T cells are likely the key effectors of PD-related neuroinflammation. These findings provide new insights into the pathogenesis and treatment options for PD, and further research and clinical trials based on the five potential drug targets and neuroinflammation are necessary.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"7380-7392"},"PeriodicalIF":4.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143075269","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":"The Potential of Mitochondrial Therapeutics in the Treatment of Oxidative Stress and Inflammation in Aging.","authors":"Jitendra Kumar Sinha, Khanak Jorwal, Krishna Kumar Singh, Sung Soo Han, Rakesh Bhaskar, Shampa Ghosh","doi":"10.1007/s12035-024-04474-0","DOIUrl":"10.1007/s12035-024-04474-0","url":null,"abstract":"<p><p>Mitochondria are central to cellular energy production, and their dysfunction is a major contributor to oxidative stress and chronic inflammation, pivotal factors in aging, and related diseases. With aging, mitochondrial efficiency declines, leading to an increase in ROS and persistent inflammatory responses. Therapeutic interventions targeting mitochondrial health show promise in mitigating these detrimental effects. Antioxidants such as MitoQ and MitoVitE, and supplements like coenzyme Q10 and NAD + precursors, have demonstrated potential in reducing oxidative stress. Additionally, gene therapy aimed at enhancing mitochondrial function, alongside lifestyle modifications such as regular exercise and caloric restriction can ameliorate age-related mitochondrial decline. Exercise not only boosts mitochondrial biogenesis but also improves mitophagy. Enhancing mitophagy is a key strategy to prevent the accumulation of dysfunctional mitochondria, which is crucial for cellular homeostasis and longevity. Pharmacological agents like sulforaphane, SS-31, and resveratrol indirectly promote mitochondrial biogenesis and improve cellular resistance to oxidative damage. The exploration of mitochondrial therapeutics, including emerging techniques like mitochondrial transplantation, offers significant avenues for extending health span and combating age-related diseases. However, translating these findings into clinical practice requires overcoming challenges in precisely targeting dysfunctional mitochondria and optimizing delivery mechanisms for therapeutic agents. Continued research is essential to refine these approaches and fully understand the interplay between mitochondrial dynamics and aging.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"6748-6763"},"PeriodicalIF":4.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142126149","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":"Mitochondrial Dysfunction is a Crucial Immune Checkpoint for Neuroinflammation and Neurodegeneration: mtDAMPs in Focus.","authors":"Yogesh Mishra, Ashutosh Kumar, Ravinder Kumar Kaundal","doi":"10.1007/s12035-024-04412-0","DOIUrl":"10.1007/s12035-024-04412-0","url":null,"abstract":"<p><p>Neuroinflammation is a pivotal factor in the progression of both age-related and acute neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, multiple sclerosis, and stroke. Mitochondria, essential for neuronal health due to their roles in energy production, calcium buffering, and oxidative stress regulation, become increasingly susceptible to dysfunction under conditions of metabolic stress, aging, or injury. Impaired mitophagy in aged or injured neurons leads to the accumulation of dysfunctional mitochondria, which release mitochondrial-derived damage-associated molecular patterns (mtDAMPs). These mtDAMPs act as immune checkpoints, activating pattern recognition receptors (PRRs) and triggering innate immune signaling pathways. This activation initiates inflammatory responses in neurons and brain-resident immune cells, releasing cytokines and chemokines that damage adjacent healthy neurons and recruit peripheral immune cells, further amplifying neuroinflammation and neurodegeneration. Long-term mitochondrial dysfunction perpetuates a chronic inflammatory state, exacerbating neuronal injury and contributing additional immunogenic components to the extracellular environment. Emerging evidence highlights the critical role of mtDAMPs in initiating and sustaining neuroinflammation, with circulating levels of these molecules potentially serving as biomarkers for disease progression. This review explores the mechanisms of mtDAMP release due to mitochondrial dysfunction, their interaction with PRRs, and the subsequent activation of inflammatory pathways. We also discuss the role of mtDAMP-triggered innate immune responses in exacerbating both acute and chronic neuroinflammation and neurodegeneration. Targeting dysfunctional mitochondria and mtDAMPs with pharmacological agents presents a promising strategy for mitigating the initiation and progression of neuropathological conditions.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"6715-6747"},"PeriodicalIF":4.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141902349","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":"Plasma Metabolites as Mediators Between Gut Microbiota and Parkinson's Disease: Insights from Mendelian Randomization.","authors":"Jianzhun Chen, Liuhui Zhu, Fang Wang, Yangfan Zhu, Jieyu Chen, Chunyu Liang, Bin Liu, Ailan Pang, Xinglong Yang","doi":"10.1007/s12035-025-04765-0","DOIUrl":"10.1007/s12035-025-04765-0","url":null,"abstract":"<p><p>Recent evidence supports the causal role of both plasma metabolites and gut microbiota (GM) in Parkinson's disease (PD). However, it remains unclear whether GM are responsible for causing PD through plasma metabolites. Here, we used Mendelian randomization (MR) to investigate the intrinsic causal relationships among GM, plasma metabolites, and PD. Summary statistics were derived from a GWAS of 1400 metabolites (N = 8299), GM (N = 18,340), and PD (Ncase = 33,674 and Ncontrol = 449,056). We used two-step/mediation MR (TSMR) to study the mediating effect of plasma metabolites on the association between GM and the risk of developing PD. We detected 54 genetic traits that were causally associated with PD development. According to the TSMR analysis, ceramide had a mediating effect on the relationship between the genus Clostridium sensu stricto 1 and the risk of developing PD (15.35% mediation; 95% CI = 1.29-32.75%). 7-Alpha-hydroxy-3-oxo-4-cholestenoate had a mediating effect on the relationship between the genus Eubacterium xylanophilum group and the risk of developing PD (11.04% mediation; 95% CI = 0.11-27.07%). In the present study, we used MR analysis to investigate the connections among GM, plasma metabolites, and PD. This comprehensive investigation offers insights into the pathogenic mechanisms of PD and the roles of the intestinal microbiota and metabolites in this disease.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"7945-7956"},"PeriodicalIF":4.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143441522","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":"Nrf2 Ameliorates Sevoflurane-Induced Cognitive Deficits in Aged Mice by Inhibiting Neuroinflammation in the Hippocampus.","authors":"Junhua Li, Jinfeng Li, Yafang Liu, Chuwen Hu, Hui Xu, Dong Cao, Rong Zhang, Kun Zhang","doi":"10.1007/s12035-025-04777-w","DOIUrl":"10.1007/s12035-025-04777-w","url":null,"abstract":"<p><p>Perioperative neurocognitive disorders (PND), common complications that occur after anesthetized surgery in elderly patients, are major challenges to our rapidly growing aging population. The transcription factor known as nuclear factor erythroid-2-related factor 2 (Nrf2) is an essential component of the cellular antioxidant response, purportedly contributing to the preservation of cognitive functions such as learning and memory. Nevertheless, the function and intracellular processes involving Nrf2 in PND remain largely unknown. Therefore, we evaluate the influence and fundamental mechanism of Nrf2 on PND in aged mice. To establish the postoperative neurocognitive dysfunction (PND) model, aged mice were subjected to anesthesia via inhalation of 3% sevoflurane for a duration of 2 h. The role of Nrf2 in PND was investigated by administering microinjections of either the adeno-associated virus (AAV)-Nrf2 vector or a null virus vector into the hippocampal CA1 region of aged mice 28 days before exposure to sevoflurane. Various assays including enzyme-linked immunosorbent assay (ELISA), immunofluorescence staining, and western blotting were employed to assess levels of pro-inflammatory cytokines, microglial activation, and the oxidative stress response. Furthermore, synaptic plasticity was evaluated through long-term potentiation (LTP) recording and Golgi staining techniques. Elevated expression of Nrf2 within the hippocampal CA1 region ameliorated sevoflurane-induced cognitive deficits, synaptic plasticity anomalies, and the oxidative stress reaction in aged mice. Furthermore, the activation of microglia and the release of pro-inflammatory cytokines (including IL-6, TNF-α, and IL-1β) within the hippocampus post-sevoflurane exposure were modulated in an Nrf2-dependent fashion. Based on the findings from present research, we conclude that Nrf2 ameliorates sevoflurane-induced cognitive dysfunction by inhibiting hippocampal neuroinflammation, thereby proposing a potential therapeutic target for PND.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"8048-8064"},"PeriodicalIF":4.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143449709","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":"The Role of Cardiolipin in Brain Bioenergetics, Neuroinflammation, and Neurodegeneration.","authors":"Patrick C Bradshaw, Jessa L Aldridge, Leah E Jamerson, Canah McNeal, A Catherine Pearson, Chad R Frasier","doi":"10.1007/s12035-024-04630-6","DOIUrl":"10.1007/s12035-024-04630-6","url":null,"abstract":"<p><p>Cardiolipin (CL) is an essential phospholipid that supports the functions of mitochondrial membrane transporters and oxidative phosphorylation complexes. Due to the high level of fatty acyl chain unsaturation, CL is prone to peroxidation during aging, neurodegenerative disease, stroke, and traumatic brain or spinal cord injury. Therefore, effective therapies that stabilize and preserve CL levels or enhance healthy CL fatty acyl chain remodeling are needed. In the last few years, great strides have been made in determining the mechanisms through which precursors for CL biosynthesis, such as phosphatidic acid (PA), are transferred from the ER to the outer mitochondrial membrane (OMM) and then to the inner mitochondrial membrane (IMM) where CL biosynthesis takes place. Many neurodegenerative disorders show dysfunctional mitochondrial ER contact sites that may perturb PA transport and CL biosynthesis. However, little is currently known on how neuronal mitochondria regulate the synthesis, remodeling, and degradation of CL. This review will focus on recent developments on the role of CL in neurological disorders. Importantly, due to CL species in the brain being more unsaturated and diverse than in other tissues, this review will also identify areas where more research is needed to determine a complete picture of brain and spinal cord CL function so that effective therapeutics can be developed to restore the rates of CL synthesis and remodeling in neurological disorders.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"7022-7040"},"PeriodicalIF":4.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142667487","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":"Milnacipran and Vanillin Alleviate Fibromyalgia-Associated Depression in Reserpine-Induced Rat Model: Role of Wnt/β-Catenin Signaling.","authors":"Nour A Kamaly, Ahmed S Kamel, Nermin Abdelhamid Sadik, Nancy N Shahin","doi":"10.1007/s12035-025-04723-w","DOIUrl":"10.1007/s12035-025-04723-w","url":null,"abstract":"<p><p>Fibromyalgia (FM) patients are highly susceptible to depression. Wnt/β-catenin signaling has shown a crucial role against depression in several studies. The FDA-approved FM drug, milnacipran (Miln), has shown antinociceptive potential against FM. Yet, no study has investigated its antidepressant potential in FM. Vanillin (Van), a well-known phytochemical often employed as flavoring agent, has been previously reported for its antidepressant and antinociceptive effects in several animal models, but has not been tested so far in FM. This study explored the antidepressant effect of Van and Miln in FM through investigating Wnt/β-catenin signaling. FM was induced in female Wistar rats by injecting reserpine (1 mg/kg/day s.c) for 3 days. Thereafter, animals received either Miln (30 mg/kg/day p.o) or Van (100 mg/kg/day p.o) for the subsequent 14 days. Results showed that both drugs demonstrated antidepressant effect in forced swimming test besides analgesic, and antiallodynic influences observed in Randall-Selitto, hot plate, cold allodynia, Von-Frey, and tail immersion tests. Biochemically, Miln and Van significantly enhanced serotonergic transmission in the hippocampus and upregulated the protein expression of the Wnt/GSK-3β/β-catenin signaling axis, including the downstream proteins, T cell factor, and dicer. This is followed by subsequent upregulation of the resilience micro ribonucleic acids (miRNAs) 124 and 135. Histopathological examinations corroborated the biochemical and molecular findings. Interestingly, these effects of Miln and Van were overturned via administration of the β-catenin inhibitor, XAV939 (0.1 mg/kg, i.p., daily). In conclusion, this study outlined the antidepressant aptitude of Miln and Van through activating Wnt/β-catenin signaling in the hippocampus in reserpine-induced FM.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"7682-7705"},"PeriodicalIF":4.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12078381/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143382628","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Application of MicroRNAs in Traumatic Brain Injury: Mechanism Elucidation and Clinical Translation.","authors":"Hong Wang, Xiaolin Fan, Yuhao Zhang, Ning Ma, Liang Li, Qing Lu, Qi Wang, Boya Yu, Xiao Li, Junhong Gao","doi":"10.1007/s12035-025-04737-4","DOIUrl":"10.1007/s12035-025-04737-4","url":null,"abstract":"<p><p>Traumatic brain injury (TBI) is a complex neurological disease caused by external forces impacting the head and is one of the leading causes of mortality and disability worldwide, exerting a significant impact on public health and socioeconomic conditions. Current research on TBI has focused primarily on assessing injury severity, determining clinical treatment, and improving patient prognosis. The timely and accurate diagnosis of TBI in clinical settings and the implementation of effective therapeutic strategies remain challenging. However, a deeper understanding of changes in gene expression and underlying molecular regulatory processes may alleviate this pressing issue. MicroRNAs (miRNAs), a class of short noncoding RNA molecules, play crucial roles in cellular physiology and pathology by regulating gene expression. With advancements in research, miRNAs have garnered increasing attention in TBI studies. This review summarizes the progress of miRNA research in TBI and explores the potential of miRNAs as diagnostic and prognostic markers and therapeutic targets for TBI.</p>","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":"7846-7863"},"PeriodicalIF":4.6,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143408453","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}