Translational Stroke Research最新文献

{"title":"Blood-Brain Barrier Disruption and Imaging Assessment in Stroke.","authors":"Yuchen Liang, Yueluan Jiang, Jiaxin Liu, Xuewei Li, Xinyue Cheng, Lei Bao, Hongwei Zhou, Zhenni Guo","doi":"10.1007/s12975-024-01300-6","DOIUrl":"10.1007/s12975-024-01300-6","url":null,"abstract":"<p><p>Disruption of the blood-brain barrier (BBB) is an important pathological hallmark of ischemic stroke. Blood-brain barrier disruption (BBBD) is a consequence of ischemia and may also exacerbate damage to brain parenchyma. Therefore, maintaining BBB integrity is critical for the central nervous system (CNS) homeostasis. This review offers a concise overview of BBB structure and function, along with the mechanisms underlying its impairment following a stroke. In addition, we review the recent imaging techniques employed to study blood-brain barrier permeability (BBBP) in the context of ischemic brain injury with the goal of providing imaging guidance for stroke diagnosis and treatment from the perspective of the BBBD. This knowledge is vital for developing strategies to safeguard the BBB during cerebral ischemia.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":" ","pages":"1400-1411"},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142354505","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":"Impact of Surgical Revascularization on Regression of Enlarged Perivascular Spaces in Adult Moyamoya Disease.","authors":"Shusuke Yamamoto, Takuya Akai, Daina Kashiwazaki, Kunitaka Maruyama, Emiko Hori, Naoki Akioka, Kyo Noguchi, Satoshi Kuroda","doi":"10.1007/s12975-024-01303-3","DOIUrl":"10.1007/s12975-024-01303-3","url":null,"abstract":"<p><p>Previous studies have suggested that enlarged perivascular spaces (EPVSs) are potential radiological markers of cerebral ischemia in moyamoya disease (MMD). However, serial changes in EPVSs after surgical revascularization have not yet been clarified. We aimed to elucidate the postoperative changes in EPVSs in adult patients with MMD, clinical and radiological factors affecting the number of EPVSs, and the degree of postoperative changes. We counted the EPVSs in the centrum semiovale in each hemisphere on a T2-weighted MRI performed before surgery. EPVSs were quantified 3 months and 2 years after combined bypass surgery in surgically treated patients and compared with the number of EPVSs before surgery. We performed multivariate logistic regression analysis to identify the clinical and radiological factors associated with the number of EPVSs. This study included 120 hemispheres of 65 adults with MMD. Older age (P < 0.01), posterior cerebral artery (PCA) involvement (P < 0.01), and cerebral blood flow (CBF) impairment (P = 0.02) were significantly associated with a large number of EPVSs. The number of EPVSs markedly decreased at 3 months and 2 years after surgery compared with that before surgery (P < 0.01). PCA involvement (P = 0.04) and CBF impairment (P = 0.02) were independent predictors of the regression of EPVSs after surgery. The number of EPVSs in the centrum semiovale was closely associated with age, PCA involvement, and CBF impairment in adult patients with MMD, which remarkably regressed after surgical revascularization, especially in the hemispheres with PCA involvement and CBF impairment. EPVSs are reversible radiological markers reflecting impaired cerebral hemodynamics in adult patients with MMD.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":" ","pages":"1241-1250"},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142393548","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":"Progesterone Receptor Agonist, Nestorone, Exerts Long-Term Neuroprotective Effects Against Permanent Focal Cerebral Ischemia in Adult and Aged Male Rats.","authors":"Motoki Tanaka, Masahiro Sokabe, Masato Asai","doi":"10.1007/s12975-024-01288-z","DOIUrl":"10.1007/s12975-024-01288-z","url":null,"abstract":"<p><p>Stroke is a leading cause of death and disability worldwide. Tissue plasminogen activator (tPA) is currently the most effective medicine for stroke; however, it has a narrow therapeutic time window (4.5 h after symptom onset). We demonstrated that nestorone, a progesterone (P4) receptor agonist, exerted neuroprotective effects against transient focal cerebral ischemia 6 h post-ischemic administration in adult male rats. This study examines its effects on permanent focal cerebral ischemia in adult and aged male rats, which are better models for evaluating treatment outcomes in typical stroke patients. Adult (6-month-old) or aged (18-month-old) male rats subjected to permanent middle cerebral artery occlusion (pMCAO) were continuously administered nestorone (10µg/day) or its vehicle (30% hydroxypropyl-β-cyclodextrin) for 7 days via an osmotic pump subcutaneously implanted, starting at 18 h post-pMCAO. Nestorone-treated adult male rats showed marked improvements in behavioral outcomes in the adhesive removal and rotarod tests and a significant reduction in infarct size compared to vehicle-treated rats 9 and 30 days post-pMCAO. The same administration of nestorone resulted in apparently comparable neuroprotective effects in aged male rats. The inflammatory mediator NF-κB/p65 was increased in Iba-1 positive cells 24 h post-pMCAO, but was significantly suppressed by subcutaneous injection of nestorone. These results suggested that nestorone exerts long-term neuroprotective effects against permanent focal cerebral ischemia in adult and aged male rats. Nestorone is thus a promising agent for post-stroke treatment owing to its wide age-independent therapeutic time window (18 h after symptom onset), which is longer than that of tPA therapy.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":" ","pages":"1118-1132"},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142018706","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":"SARS-CoV-2 Spike Protein Exacerbates Thromboembolic Cerebrovascular Complications in Humanized ACE2 Mouse Model.","authors":"Stan P Heath, Veronica C Hermanns, Maha Coucha, Mohammed Abdelsaid","doi":"10.1007/s12975-024-01301-5","DOIUrl":"10.1007/s12975-024-01301-5","url":null,"abstract":"<p><p>COVID-19 increases the risk for acute ischemic stroke, yet the molecular mechanisms are unclear and remain unresolved medical challenges. We hypothesize that the SARS-CoV-2 spike protein exacerbates stroke and cerebrovascular complications by increasing coagulation and decreasing fibrinolysis by disrupting the renin-angiotensin-aldosterone system (RAAS). A thromboembolic model was induced in humanized ACE2 knock-in mice after one week of SARS-CoV-2 spike protein injection. hACE2 mice were treated with Losartan, an angiotensin receptor (AT₁R) blocker, immediately after spike protein injection. Cerebral blood flow and infarct size were compared between groups. Vascular-contributes to cognitive impairments and dementia was assessed using a Novel object recognition test. Tissue factor-III and plasminogen activator inhibitor-1 were measured using immunoblotting to assess coagulation and fibrinolysis. Human brain microvascular endothelial cells (HBMEC) were exposed to hypoxia with/without SARS-CoV-2 spike protein to mimic ischemic conditions and assessed for inflammation, RAAS balance, coagulation, and fibrinolysis. Our results showed that the SARS-CoV-2 spike protein caused an imbalance in the RAAS that increased the inflammatory signal and decreased the RAAS protective arm. SARS-CoV-2 spike protein increased coagulation and decreased fibrinolysis when coincident with ischemic insult, which was accompanied by a decrease in cerebral blood flow, an increase in neuronal death, and a decline in cognitive function. Losartan treatment restored RAAS balance and reduced spike protein-induced effects. SARS-CoV-2 spike protein exacerbates inflammation and hypercoagulation, leading to increased neurovascular damage and cognitive dysfunction. However, the AT₁R blocker, Losartan, restored the RAAS balance and reduced COVID-19-induced thromboembolic cerebrovascular complications.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":" ","pages":"1214-1228"},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11973837/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142362138","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":"Serum Metabolome Profiling Reveals Biomarkers to Predict Malignant Brain Edema Following Endovascular Stroke Therapy.","authors":"Jiaqi Luo, Xiaolin Zhao, Mengxuan Xiao, Junlin Deng, Shuhua Xie, Huanhuan Fan, Wenting Lu, Yuqing Su, Tong Wu, Huanrong Ma, Xianghong Liu, Suyue Pan, Kaibin Huang","doi":"10.1007/s12975-025-01372-y","DOIUrl":"https://doi.org/10.1007/s12975-025-01372-y","url":null,"abstract":"<p><p>Metabolomics reflects the body's metabolic state and holds substantial promise for identifying associated biomarkers and exploring pathological processes. This study used serum metabolomics to predict malignant brain edema (MBE) following endovascular therapy (EVT) for acute ischemic stroke (AIS) and investigate the underlying mechanisms. In this prospective observational study, we enrolled patients with anterior circulation large vessel occlusion who underwent successful recanalization post-EVT for AIS, including those with or without concomitant hemorrhagic transformation. Eligible patients were stratified into two groups according to the subsequent presence of MBE. Following propensity score matching to adjust for potential confounders, widely targeted metabolomic analysis was conducted on the serum samples. A prediction model, based on the identified differential metabolites, was then developed and validated in another independent cohort. Through widely targeted metabolomic analysis of serum samples from matched 46 patients, we identified 30 metabolites that were significantly altered between patients with and without MBE, including notable differences in acylcarnitine, lysophosphatidylcholine, riboflavin, and tyrosine. A prediction model incorporating 9 differential metabolites was constructed using 10-fold frame shift cross-validation, demonstrating prediction performance in the training set, test set, and external validation, with areas under the curve (AUC) of 0.842, 0.815, and 0.734, respectively. Dynamic change analysis based on multiple time points may suggest a potential role of diminished oxidative energy supply and sustained stress in MBE. The identified acylcarnitine and lysophosphatidylcholine might play influential roles in the pathogenesis of MBE. The prediction model derived from these differential metabolites holds promise as a noninvasive assay for the early detection of MBE and warrants additional refinement and validation.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144761437","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":"Changes in Neuroimmunological Synapses During Cerebral Ischemia.","authors":"Lynn Bitar, Berta Puig, Thomas G Oertner, Ádám Dénes, Tim Magnus","doi":"10.1007/s12975-024-01286-1","DOIUrl":"10.1007/s12975-024-01286-1","url":null,"abstract":"<p><p>The direct interplay between the immune and nervous systems is now well established. Within the brain, these interactions take place between neurons and resident glial cells, i.e., microglia and astrocytes, or infiltrating immune cells, influenced by systemic factors. A special form of physical cell-cell interactions is the so-called \"neuroimmunological (NI) synapse.\" There is compelling evidence that the same signaling pathways that regulate inflammatory responses to injury or ischemia also play potent roles in brain development, plasticity, and function. Proper synaptic wiring is as important during development as it is during disease states, as it is necessary for activity-dependent refinement of neuronal circuits. Since the process of forming synaptic connections in the brain is highly dynamic, with constant changes in strength and connectivity, the immune component is perfectly suited for the regulatory task as it is in constant turnover. Many cellular and molecular players in this interaction remain to be uncovered, especially in pathological states. In this review, we discuss and propose possible communication hubs between components of the adaptive and innate immune systems and the synaptic element in ischemic stroke pathology.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":" ","pages":"1369-1382"},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12202685/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141894335","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":"A Randomised Controlled Trial of SFX-01 After Subarachnoid Haemorrhage - The SAS Study.","authors":"Ardalan Zolnourian, Patrick Garland, Patrick Holton, Mukul Arora, Jonathan Rhodes, Christopher Uff, Tony Birch, David Howat, Stephen Franklin, Ian Galea, Diederik Bulters","doi":"10.1007/s12975-024-01278-1","DOIUrl":"10.1007/s12975-024-01278-1","url":null,"abstract":"<p><p>SFX-01 is a novel drug for clinical delivery of sulforaphane (SFN). SFN is a potent nuclear factor erythroid 2-related factor 2 activator that reduces inflammation and oxidation, improving outcomes after subarachnoid haemorrhage (SAH) in animal models. This was a multi-centre, double-blind, placebo-controlled, parallel-group randomised clinical trial to evaluate the safety, pharmacokinetics and efficacy of 28 days of SFX-01 300 mg BD in patients aged 18-80 with spontaneous SAH and high blood load on CT. Primary outcomes were (1) safety, (2) plasma and CSF SFN and metabolite levels and (3) vasospasm on transcranial doppler ultrasound. Secondary outcomes included CSF haptoglobin and malondialdehyde and clinical outcome on the modified Rankin Scale (mRS) and SAH outcome tool (SAHOT). A total of 105 patients were randomised (54 SFX-01, 51 placebo). There were no differences in adverse events other than nausea (9 SFX-01 (16.7%), 1 placebo (2.0%)). SFN, SFN-glutathione and SFN-N-acetyl-cysteine AUC_last were 16.2, 277 and 415 h × ng/ml. Plasma SFN was higher in GSTT1 null individuals (t = 2.40, p = 0.023). CSF levels were low with many samples below the lower limit of quantification and predicted by the CSF/serum albumin ratio (R² = 0.182, p = 0.039). There was no difference in CSF haptoglobin (1.981 95%CI 0.992-3.786, p = 0.052) or malondialdehyde (1.12 95%CI 0.7477-1.687, p = 0.572) or middle cerebral artery flow velocity (1.04 95%CI 0.903-1.211, p = 0.545) or functional outcome (mRS 1.647 95%CI 0.721-3.821, p = 0.237, SAHOT 1.082 95%CI 0.464-2.525, p = 0.855). SFX-01 is safe and effective for the delivery of SFN in acutely unwell patients. SFN penetrated CSF less than expected and did not reduce large vessel vasospasm or improve outcome. Trial registration: NCT02614742 clinicaltrials.gov.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":" ","pages":"1031-1043"},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12202693/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141724578","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":"Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1 (LOX-1): A Potential Therapeutic Target in Ischemic Stroke.","authors":"Yue Hu, Yuhao Li, Yumin Luo, Ningqun Wang, Yangmin Zheng","doi":"10.1007/s12975-024-01307-z","DOIUrl":"10.1007/s12975-024-01307-z","url":null,"abstract":"<p><p>Stroke, the leading cause of disability and the second leading cause of death worldwide, is characterized by high morbidity and disability. The lectin-like oxidized low-density lipoprotein receptor (LOX-1) is a scavenger receptor that promotes endothelial dysfunction by recognizing and internalizing oxidized low-density lipoproteins (ox-LDL) to induce the formation, development, and instability of atherosclerotic plaques, ultimately leading to vascular thrombosis. Previous clinical and epidemiological studies have indicated that LOX-1 plays a vital role in cerebral ischemic injury following ischemic stroke. Multiple clinical studies have shown that the genetic polymorphisms in LOX-1 are associated with susceptibility to ischemic stroke. Soluble LOX-1 (sLOX-1), a biomarker of ischemic stroke, is associated with the prognosis of ischemic stroke. This article discusses the clinical and experimental findings on LOX-1 in ischemic stroke and the development of new therapeutic strategies targeting LOX-1.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":" ","pages":"1412-1423"},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12202518/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142688713","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 Role of Complement C1qa in Experimental Intracerebral Hemorrhage.","authors":"Xiongjie Fu, Fenghui Ye, Yingfeng Wan, Guohua Xi, Ya Hua, Richard F Keep","doi":"10.1007/s12975-024-01302-4","DOIUrl":"10.1007/s12975-024-01302-4","url":null,"abstract":"<p><p>Evidence indicates that the complement system is activated and plays a role in brain injury after intracerebral hemorrhage (ICH). Most studies have focused on the role of C3, C5 and the membrane attack complex. The purpose of this study was to investigate the potential impact of complement C1q, a key upstream component of the classical pathway, on ICH-induced brain injury. Wild-type (WT) and C1qa knock out (KO) mice were compared using an autologous blood injection ICH model. Magnetic resonance imaging (MRI) was performed on days 1, 3 and 7 and brains harvested on days 3 and 7 for immunohistochemistry to examine brain injury mechanisms. WT and C1qa KO mice also received an intracerebral injection of thrombin, a key factor in ICH-induced brain injury. Following MRI scans, brains were harvested for immunohistochemistry on day 1. In comparison to WT mice, C1qa KO mice had reduced hematoma erythrolysis and neutrophil infiltration after ICH. However, they also had delayed hematoma clearance, which was associated with reduced induction of phagocytic multinuclear giant cells, and increased perihematomal neuronal damage. After thrombin injection, C1qa KO mice had smaller lesion volumes, less neuronal loss, reduced neutrophil infiltration, and less BBB damage. C1qa knockout has beneficial and detrimental effects on ICH-induced brain injury mechanisms, but a consistent beneficial effect after thrombin injection. Strategies to balance the roles of C1q after ICH may represent a promising therapeutic direction.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":" ","pages":"1229-1240"},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142381705","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":"RNF213 p.Arg4810Lys Variant Is Associated with Higher Stenosis Progression in Asymptomatic Intracranial Artery Stenosis.","authors":"Shogo Dofuku, Satoru Miyawaki, Hideaki Imai, Masahiro Shimizu, Hiroki Hongo, Yuki Shinya, Kenta Ohara, Yu Teranishi, Hideaki Ono, Hirofumi Nakatomi, Akira Teraoka, Nobuhito Saito","doi":"10.1007/s12975-024-01309-x","DOIUrl":"10.1007/s12975-024-01309-x","url":null,"abstract":"<p><p>Intracranial artery stenosis (ICAS) is a significant contributor to ischemic stroke, with the RNF213 p.Arg4810Lys variant identified as a related genetic factor. We explored the clinical outcomes of the RNF213 genotype in patients with asymptomatic ICAS. Between November 2011 and March 2019, 139 patients with asymptomatic ICAS were enrolled in this study. Genotyping for RNF213 p.Arg4810Lys was performed using Sanger sequencing. A comprehensive analysis was conducted to compare the RNF213 genotype with background characteristics and clinical outcomes such as ipsilateral ischemic cerebrovascular events and stenosis progression. RNF213 p.Arg4810Lys was found in 25% of cases, revealing distinct clinical features between carriers and non-carriers. The incidence of ipsilateral ischemic cerebrovascular events was 4.3% (6/139 cases), and stenosis progression was observed in 13% (18/139 cases) during a mean follow-up period of 58 months. Stenosis progression rates were notably higher in the RNF213 variant group (25.7%; 9/35 cases) than in the RNF213 wild-type group (8.7%; 9/104 cases). Cumulative stenosis progression rate was significantly higher in the RNF213 variant group than in the RNF213 wild-type group (log-rank test, P = 0.0004). Multivariate Cox regression analysis indicated a significant association between the RNF213 p.Arg4810Lys variant and an increased risk of stenosis progression (P = 0.03, odds ratio 3.2; 95% confidence interval, 1.1-9.0). The RNF213 p.Arg4810Lys variant exhibits clinical disparities in asymptomatic ICAS and is notably linked to a heightened risk of stenosis progression. These results suggest a distinct difference in the vascular stenosis mechanism associated with this variant, warranting further investigation into its clinical implications and potential mechanistic insights.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":" ","pages":"1293-1300"},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12202689/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142628955","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}