Translational Stroke Research最新文献

{"title":"Targeted TGF-βR2 Silencing in the Retrotrapezoid Nucleus Mitigates Respiratory Dysfunction and Cognitive Decline in a Mouse Model of Cerebral Amyloid Angiopathy with and without Stroke.","authors":"Ahmad El Hamamy, Zahid Iqbal, Ngoc Mai Le, Arya Ranjan, YuXing Zhang, Hung Wen Lin, Chunfeng Tan, Destiny Sumani, Anthony Patrizz, Louise D McCullough, Jun Li","doi":"10.1007/s12975-024-01306-0","DOIUrl":"10.1007/s12975-024-01306-0","url":null,"abstract":"<p><p>Cerebral amyloid angiopathy (CAA) is characterized by the deposition of amyloid-beta peptides within cerebral blood vessels, leading to neurovascular complications. Ischemic strokes result from acute disruptions in cerebral blood flow, triggering metabolic disturbances and neurodegeneration. Both conditions often co-occur and are associated with respiratory dysfunctions. The retrotrapezoid nucleus (RTN), which is crucial for CO₂ sensing and breathing regulation in the brainstem, may play a key role in breathing disorders seen in these conditions. This study aims to investigate the role of Transforming Growth Factor Beta (TGF-β) signaling in the RTN on respiratory and cognitive functions in CAA, both with and without concurrent ischemic stroke. Adult male Tg-SwDI (CAA model) mice and C57BL/6 wild-type controls underwent stereotaxic injections of lentivirus targeting TGF-βR2 in the RTN. Stroke was induced by middle cerebral artery occlusion using a monofilament. Respiratory functions were assessed using whole-body plethysmography, while cognitive functions were evaluated through the Barnes Maze and Novel Object Recognition Test (NORT). Immunohistochemical analysis was conducted to measure TGF-βR2 and GFAP expressions in the RTN. CAA mice exhibited significant respiratory dysfunctions, including reduced respiratory rates and increased apnea frequency, as well as impaired cognitive performance. TGF-βR2 silencing in the RTN improved respiratory functions and cognitive outcomes in CAA mice. In CAA mice with concurrent stroke, TGF-βR2 silencing similarly enhanced respiratory and cognitive functions. Immunohistochemistry confirmed reduced TGF-βR2 and GFAP expressions in the RTN following silencing. Our findings demonstrate that increased TGF-β signaling and gliosis in the RTN contribute to respiratory and cognitive dysfunctions in CAA and CAA with stroke. Targeting TGF-βR2 signaling in the RTN offers a promising therapeutic strategy to mitigate these impairments. This study is the first to report a causal link between brainstem gliosis and both respiratory and cognitive dysfunctions in CAA and stroke models.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":" ","pages":"1272-1284"},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142628956","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":"Cilostazol Alleviates Delayed Cerebral Ischemia After Subarachnoid Hemorrhage by Attenuating Microcirculatory Dysfunction.","authors":"Masato Naraoka, Norihito Shimamura, Hiroki Ohkuma","doi":"10.1007/s12975-024-01308-y","DOIUrl":"10.1007/s12975-024-01308-y","url":null,"abstract":"<p><p>Cilostazol, a phosphodiesterase 3 (PDE3) inhibitor that exerts antiplatelet effects, has therapeutic potential for delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (aSAH). However, its mechanism of action remains unclear. We hypothesized that cilostazol alleviates DCI by improving cerebral microcirculatory dysfunction, which is a component of early brain injury. To test this hypothesis, we analyzed the intracerebral circulation time (iCCT) in 256 patients with aSAH from two randomized controlled trials (74 received cilostazol, 54 received pitavastatin, and 128 were controls). A minority of patients (n = 72, 28%) developed severe angiographic vasospasm (aVS) and DCI (n = 42, 16%) and had poor outcomes (n = 35, 14%). We measured iCCT as the time to peak in the ultraearly phase (baseline) and the subacute phase or at DCI onset (follow-up). The cilostazol group had shorter follow-up iCCT and larger iCCT differences than the other groups, indicating improved microcirculatory function, particularly in patients with DCI and poor outcomes. Multivariate analysis revealed that cilostazol treatment is a significant predictor of favorable outcomes, whereas DCI occurrence, a decrease in iCCT differences, and high clinical severity (Hunt & Hess grades 3-4) were associated with poor outcomes. Diminished microcirculatory dysfunction may alleviate DCI and improve outcomes among patients with aSAH following cilostazol treatment. Further research is warranted to confirm these findings and explore the dose-dependent effects of cilostazol on the microcirculatory function.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":" ","pages":"1285-1292"},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142676690","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":"Catecholamine-Induced Inflammasome Activation in the Heart Following Photothrombotic Stroke.","authors":"Xavier O Scott, Nadine A Kerr, Juliana Sanchez-Molano, Juan Pablo de Rivero Vaccari, Roey Hadad, Alicia De La Cruz, H Peter Larsson, W Dalton Dietrich, Robert W Keane","doi":"10.1007/s12975-024-01311-3","DOIUrl":"10.1007/s12975-024-01311-3","url":null,"abstract":"<p><p>Cerebrovascular stroke patients exhibit an increased incidence of cardiac arrhythmias. The pathomechanisms underlying post-traumatic cardiac dysfunction include a surge of catecholamines and an increased systemic inflammatory response, but whether inflammasome activation contributes to cardiac dysfunction remains unexplored. Here, we used a mouse model of photothrombotic stroke (PTS) to investigate the role of inflammasome activation in post-stroke cardiac dysfunction by catecholamines and to evaluate the effectiveness of the inflammasome inhibitor IC100 on inflammasome activation. To evaluate functional electrophysiological changes in the heart by catecholamine treatment, we recorded action potential duration in excised zebrafish hearts with and without IC100 treatment. We show that PTS induced AIM2 inflammasome activation in atria and ventricles that was significantly reduced by administration of IC100. Injection of epinephrine into naïve mice induced a significant increase in AIM2, IL-1b and caspase-8 in atria. Treatment of excised zebrafish hearts with epinephrine shortened the action potential duration and this shortening that was reduced by IC100. These findings indicate that stroke initiates a catecholamine surge that induces inflammasome activation and pyroptosis in the heart that is blocked by IC100, thus providing a framework for the development of therapeutics for stroke-related cardiovascular injury.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":" ","pages":"1317-1330"},"PeriodicalIF":4.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12202682/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142648935","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":"An Alternative Photothrombotic Model of Transient Ischemic Attack.","authors":"Y N Kalyuzhnaya, A K Logvinov, S G Pashkevich, N V Golubova, E S Seryogina, E V Potapova, V V Dremin, A V Dunaev, S V Demyanenko","doi":"10.1007/s12975-024-01285-2","DOIUrl":"10.1007/s12975-024-01285-2","url":null,"abstract":"<p><p>Animal models mimicking human transient ischemic attack (TIA) and cerebral microinfarcts are essential tools for studying their pathogenetic mechanisms and finding methods of their treatment. Despite its advantages, the model of single arteriole photothrombosis requires complex experimental equipment and highly invasive surgery, which may affect the results of further studies. Hence, to achieve high translational potential, we focused on developing a TIA model based on photothrombosis of arterioles to combine good reproducibility and low invasiveness. For the first time, noninvasive laser speckle contrast imaging (LSCI) was used to monitor blood flow in cerebral arterioles and reperfusion was achieved. We demonstrate that irradiation of mouse cerebral cortical arterioles using a 532-nm laser with a 1-mm-wide beam at 2.4 or 3.7 mW for 55 or 40 s, respectively, after 15 mg/kg intravenous Rose Bengal administration, induces similar ischemia-reperfusion lesions resulting in microinfarct formation. The model can be used to study the pathogenesis of spontaneously developing cerebral microinfarcts in neurodegeneration. Reducing the exposure times by 10 s while maintaining the same other parameters caused photothrombosis of the arteriole with reperfusion in less than 1 h. This mode of photodynamic exposure caused cellular and subcellular level ischemic changes in neurons and promoted the activation of astrocytes and microglia in the first day after irradiation, but not later, without the formation of microinfarcts. This mode of photodynamic exposure most accurately reproduced human TIA, characterized by the absence of microinfarcts.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":" ","pages":"1106-1117"},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141789091","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":"Correction to: Blood DNA Methylation Analysis Reveals a Distinctive Epigenetic Signature of Vasospasm in Aneurysmal Subarachnoid Hemorrhage.","authors":"Isabel Fernández-Pérez, Joan Jiménez-Balado, Adrià Macias-Gómez, Antoni Suárez-Pérez, Marta Vallverdú-Prats, Alberto Pérez-Giraldo, Marc Viles-García, Julia Peris-Subiza, Sergio Vidal-Notari, Eva Giralt-Steinhauer, Daniel Guisado-Alonso, Manel Esteller, Ana Rodriguez-Campello, Jordi Jiménez-Conde, Angel Ois, Elisa Cuadrado-Godia","doi":"10.1007/s12975-024-01281-6","DOIUrl":"10.1007/s12975-024-01281-6","url":null,"abstract":"","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":" ","pages":"1440"},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141735104","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":"Novel Rat Model of Embolic Cerebral Ischemia Using a Radiopaque Blood Clot and a Microcatheter Under Fluoroscopy.","authors":"Teppei Komatsu, Hiroki Ohta, Misato Takeda, Yasuhiro Matsumura, Masayuki Yokoyama, Zuojun Wang, Hirotaka James Okano, Yasuyuki Iguchi","doi":"10.1007/s12975-024-01312-2","DOIUrl":"10.1007/s12975-024-01312-2","url":null,"abstract":"<p><p>Conventional rat models of thromboembolic stroke do not allow control of infarct size or spontaneous recanalization. We aimed to develop a novel rat thromboembolic stroke model that ensures highly reproducible infarct sizes and locations within the MCA territory and does not require arterial ligation. Twenty male Sprague-Dawley rats and two sham-operated rats were included. A microcatheter was navigated from the caudal ventral artery to the internal carotid artery using digital subtraction angiography. A blood clot (diameter, 0.86 mm; length, 3 mm) containing zirconium dioxide was advanced in the catheter. Fluoroscopy was performed at 1, 3, 6, and 24 h after stroke model creation, and TTC staining was conducted at 24 h. Neurological deficit scores were measured. In all embolized rats, the ACA and MCA bifurcation were selective. Median operating time was 6 min. The position of the radiopaque blood clot remained unchanged for 24 h after model creation in 19/20 rats. Median infarct volume was 242 mm³ (IQR, 239-262 mm³). We present a novel rat model of highly reproducible focal infarct in only the MCA territory. Fluoroscopy effectively identified any blood clot migration. This model could contribute to the development of new thrombolytic agents.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":" ","pages":"1331-1339"},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142668232","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":"Enlarged Perivascular Spaces (EPVS) Associated with Functional and Cognitive Outcome After Aneurysm Subarachnoid Hemorrhage (aSAH).","authors":"Haichao Wang, Qiuyue Yu, Wenyi Zhang, Shengqi Yao, Yun Zhang, Qiong Dong, Yichen Zhao, Jinxing Lin, Xueyuan Liu, Li Gong","doi":"10.1007/s12975-024-01315-z","DOIUrl":"10.1007/s12975-024-01315-z","url":null,"abstract":"<p><p>Aneurysmal rupture is the main cause of subarachnoid hemorrhage (SAH), leading to neurological and cognitive deficits. The clinical significance of enlarged perivascular spaces (EPVS) on aSAH (aneurysm subarachnoid hemorrhage) outcomes was unclear. Our aim was to explore the association between EPVS and the clinical outcomes of aSAH. Magnetic resonance imaging (MRI) scans of 195 aSAH survivors were analyzed. Poor outcome was defined as modified Rankin Scale (mRS) ≥ 3. Cognitive outcomes were measured with the Montreal Cognitive Assessment (MoCA). We compared the clinical characteristics of aSAH with EPVS < 10 and EPVS ≥ 10 in basal ganglia (BG) and centrum semiovale (CSO) and investigated the association of EPVS severity and topography with delayed cerebral ischemia (DCI), subacute hydrocephalus, and 3-month unfavorable functional outcome and cognitive status using binary logistic regression model, respectively. At 3 months, 159 patients completed the MoCA assessments, and 63 (39.6%) were diagnosed with cognitive impairment (MoCA < 22). BG-EPVS ≥ 10 was associated with unfavorable functional outcomes at 3 months (odds ratio [OR] 2.426, 95% confidence interval [CI] 1.128-5.216, p < 0.05), subacute hydrocephalus (OR 3.789, 95% CI 1.049-13.093, p < 0.05), and DCI (OR 2.579, 95% CI 1.086-6.123, p < 0.05), but not with cognitive impairment after adjusting for established predictors. CSO-EPVS was linked to unfavorable functional outcomes at 3 months (OR 3.411, 95% CI 1.422-8.195, p < 0.05) and worse cognitive function (OR 2.520, 95% CI 1.136-5.589, p < 0.05). Our cohort study reveals that both BG-EPVS and CSO-EPVS are independently associated with unfavorable functional outcomes after aSAH. However, only CSO-EPVS, not BG-EPVS, is related to cognitive impairment at 3 months.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":" ","pages":"1358-1368"},"PeriodicalIF":3.8,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142830011","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":"High Plasma Sarcosine Levels Are Associated with Decreased Risks of Adverse Outcomes After Ischemic Stroke: A Multicenter Prospective Study.","authors":"Lulu Sun, Daoxia Guo, Xinyue Chang, Yi Liu, Yu He, Pinni Yang, Mengyao Shi, Jing Chen, Aili Wang, Yonghong Zhang, Jiang He, Tan Xu, Zhengbao Zhu","doi":"10.1007/s12975-025-01370-0","DOIUrl":"https://doi.org/10.1007/s12975-025-01370-0","url":null,"abstract":"<p><p>Sarcosine has been reported to improve ischemic tolerance in animal models of brain ischemia, but population-based evidence from patients with ischemic stroke is lacking. We conducted a multicenter prospective study to investigate the associations between plasma sarcosine levels and adverse outcomes among patients with ischemic stroke. We measured plasma sarcosine levels among 3473 patients with ischemic stroke from 26 hospitals across China. The primary outcome was the composite outcome of death or major disability (modified Rankin Scale [mRS] score, 3-6) at 3 months after ischemic stroke. Secondary outcomes were major disability (mRS score, 3-5), death (mRS score, 6), and cardiovascular events. During 3 months of follow-up, 853 participants experienced the primary outcome. Compared with the lowest quartile of sarcosine, the multivariable-adjusted odds ratios or hazard ratios of the highest quartile were 0.59 (P_trend < 0.001) for primary outcome, 0.70 (P_trend = 0.002) for major disability, 0.20 (P_trend < 0.001) for death, and 0.43 (P_trend = 0.017) for cardiovascular events. Multivariable-adjusted spline regression model showed linear associations of sarcosine with adverse outcomes (all P_linearity < 0.05). Adding sarcosine to conventional prognostic factors modestly improved the risk reclassification of adverse outcomes after ischemic stroke, as evidenced by net reclassification improvement and integrated discrimination improvement (all P < 0.05). Additionally, there was a strong combined effect of sarcosine and glycine on the risks of adverse outcomes after ischemic stroke. High plasma sarcosine levels were associated with low risks of adverse outcomes after ischemic stroke, suggesting that sarcosine might serve as a valuable prognostic biomarker for ischemic stroke.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":" ","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144733449","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":"FLT1 as a Protective Factor in Ischemic Stroke: Insights from Real-World Pharmacovigilance and Genetic Evidence.","authors":"Haohao Chen, Jinhua Yang, Zihao Li, Fenfei Gao","doi":"10.1007/s12975-025-01369-7","DOIUrl":"https://doi.org/10.1007/s12975-025-01369-7","url":null,"abstract":"<p><p>Ischemic stroke contributes substantially to global death and disability, yet effective molecular targets remain scarce. This study integrates real-world pharmacovigilance data, molecular databases, and genetic evidence to support the discovery and validation of novel therapeutic targets. A stepwise analytic pipeline combined adverse event signals from the FDA Adverse Event Reporting System (FAERS), drug-target data from DrugBank, and Mendelian randomization (MR) using proteomic instruments from the UK Biobank Pharma Proteomics Project (UKB PPP). Disproportionality analyses identified drugs with signals for ischemic stroke. The top 30 drugs were cross-referenced in DrugBank to identify molecular targets, which were subjected to protein interaction and pathway enrichment analyses. MR analysis assessed the causal effects of plasma proteins on ischemic stroke using GWAS data from GIGASTROKE (discovery) and FinnGen (validation). Among 88,313 ischemic stroke-related reports in FAERS, 701 drugs showed consistent signals, with the top 30 prioritized for target identification. FLT1 was the only overlapping protein between MR-significant proteins and FAERS-associated drug targets. MR analysis showed a significant inverse causal relationship between plasma FLT1 levels and ischemic stroke in both the discovery (OR, 0.864; 95% CI, 0.774-0.965) and validation (OR, 0.829; 95% CI, 0.788-0.871) datasets. FLT1 was enriched in pathways such as MAPK and PI3K-Akt, implicated in stroke-related molecular processes. FLT1 was identified as a potential protective factor against ischemic stroke through a triangulated approach combining pharmacovigilance, target bioinformatics, and MR analysis. These findings offer mechanistic insights and a promising direction for targeted intervention.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144660354","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":"Modified Intracranial Aneurysm Rupture Rat Model with Angiographic Imaging.","authors":"William Wei-Lin Pan, Masahiko Itani, Kostadin Karagiozov, Teppei Komatsu, Hiroki Ohta, Hirokazu Koseki, Shunsuke Hataoka, Yoshiki Arakawa, Hirotaka James Okano, Tomohiro Aoki, Yuichi Murayama","doi":"10.1007/s12975-025-01366-w","DOIUrl":"https://doi.org/10.1007/s12975-025-01366-w","url":null,"abstract":"<p><p>Intracranial aneurysms (IAs) are a major cause of spontaneous subarachnoid hemorrhage (SAH) and are associated with high morbidity and mortality. Current IA rodent models often exhibit low rupture rates and limited imaging capabilities, restricting their translational utility. This study introduces a modified elastase-based rat model that incorporates angiographic imaging to overcome these challenges. IAs were induced in 7-week-old female Sprague-Dawley rats using a combination of surgical and pharmacological interventions, including carotid artery and renal artery ligation, bilateral ovariectomy, high-salt diet, and two elastase injections into the basal cistern. Digital subtraction angiography (DSA) was employed to assess aneurysm formation and rupture rate. Histological and immunohistochemical analyses were conducted to characterize aneurysm morphology and the inflammatory response. The modified model achieved a high rate of IA formation (85%) and rupture (60%) within 28 days. DSA enabled visualization of vessel tortuosity and flow dynamics, features relevant to human IA development, which often occurs in areas subjected to hemodynamic stress, and the tortuosity of intracranial vessels affects their rupture ^[1]. Histological analysis indicated structural degradation of the aneurysm wall, while immunohistochemistry showed neutrophil infiltration, potentially implicating inflammation in IA rupture. This improved IA model offers a reliable method for inducing and visualizing IAs with a high rupture rate, making it a valuable tool for studying the pathophysiology and therapeutic interventions of IAs. Enhanced by DSA, this model has the potential to advance therapeutic research by enabling the real-time monitoring of aneurysm development and rupture.</p>","PeriodicalId":23237,"journal":{"name":"Translational Stroke Research","volume":" ","pages":""},"PeriodicalIF":3.8,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144650632","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}