Current neurovascular research最新文献

{"title":"Role of Miro1 in Mitochondrial Dysfunction and Neurodegeneration in Huntington's Disease.","authors":"Mustak Ahamed, Khadga Raj Aran","doi":"10.2174/0115672026501524261001101908","DOIUrl":"https://doi.org/10.2174/0115672026501524261001101908","url":null,"abstract":"<p><strong>Introduction: </strong>Huntington's Disease (HD) is an autosomal dominant neurodegenerative disorder that is caused by expansion of Cytosine-Adenine-Guanine (CAG) repeats in the Huntingtin (HTT) gene and leads to progressive motor, cognitive, and psychiatric dysfunction. Mitochondrial dysfunction is a major pathological feature of HD. Mitochondrial Rho GTPase 1 (Miro1) controls mitochondrial trafficking, calcium homeostasis, mitophagy, and neuronal signaling, and its dysregulation may contribute significantly to the progression of HD.</p><p><strong>Methods: </strong>The literature search to identify relevant studies on Miro1 biology, mitochondrial dysfunction, mitophagy, neuroinflammation, and emerging therapeutic strategies in HD followed a narrative review of the PubMed, Scopus, ScienceDirect, and Google Scholar databases. Original research articles, review articles, and preclinical studies published in English were screened for relevance, and the retrieved evidence was critically synthesized to provide an updated overview of Miro1's role in HD pathogenesis and its therapeutic potential.</p><p><strong>Results: </strong>Mutant Huntingtin (mHTT) perturbs Miro1-dependent mitochondrial transport, which leads to mitochondrial mislocalization, defective mitophagy, oxidative stress, and synaptic dysfunction. Miro1 dysregulation also facilitates neuroinflammatory signaling and neuronal vulnerability. Advances in AI have led to improved early diagnosis of HD through neuroimaging and digital biomarkers. Emerging therapies targeting Miro1, including gene therapy, nanocarriers, and pharmacological modulators, show promising neuroprotective potential in preclinical models.</p><p><strong>Discussion and conclusion: </strong>Miro1 is a potentially important molecular link between mitochondrial dysfunction and neurodegeneration in HD. Targeting Miro1-mediated pathways may restore mitochondrial homeostasis and may be a promising therapeutic strategy for disease modification.</p>","PeriodicalId":93965,"journal":{"name":"Current neurovascular research","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149170898","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neurovascular Modulation of the Blood-brain Barrier Using Focused Ultrasound for Antisense Therapy Delivery in Amyotrophic Lateral Sclerosis.","authors":"Sujit Kumar Mohanty, M K Vijayalakshmi, Sambasivam Gopinath, J Jaisudha, Deepak Venkatraman, Tozer Meena Sandela, Vasanth Kumar Mohan","doi":"10.2174/0115672026509618261001075016","DOIUrl":"https://doi.org/10.2174/0115672026509618261001075016","url":null,"abstract":"<p><strong>Introduction: </strong>Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease, and the blood-brain barrier (BBB) restricts CNS delivery of macromolecular therapeutics such as antisense oligonucleotides (ASOs). Focused ultrasound (FUS) with microbubbles enables transient, noninvasive opening of the BBB for deliver SOD1-targeted ASOs.</p><p><strong>Methods: </strong>A narrative review of the literature in PubMed, Scopus, Web of Science, and Google Scholar (2020-2025) was conducted to evaluate FUS-assisted delivery of SOD1-targeted ASOs, with an emphasis on lipid- and calcium phosphate (CaP)- based nanoparticles.</p><p><strong>Results: </strong>Preclinical studies showed that FUS-mediated BBB opening (250 kHz; mechanical index 0.33; 30-s exposure; 0.15 mL/kg microbubbles) increased brain accumulation of nanoparticle- encapsulated ASOs by >3.5-fold compared with FUS without microbubbles. CaP lipid nanoparticles (~73 nm; -21 mV; 23-30% encapsulation efficiency) encapsulating tofersen demonstrated pH-responsive intracellular release. In wild-type and G93A SOD1 transgenic mice, FUS combined with CaP-ASO nanoparticles reduced SOD1 expression in sonicated cortical regions and increased lumbar spinal motor-neuron counts without detectable neuroinflammation or tissue damage.</p><p><strong>Discussion: </strong>Combining FUS-mediated BBB modulation with CaP nanoparticles provides a minimally invasive strategy for CNS ASO delivery. Observed spinal cord effects suggest wider CNS distribution, potentially involving CSF transport and retrograde axonal pathways. Clinical translation requires optimising FUS parameters, conducting long-term safety assessments, and managing skull acoustic variability.</p><p><strong>Conclusion: </strong>MRI-guided FUS combined with CaP lipid nanoparticles represents a promising non-invasive platform for SOD1-targeted ASO delivery and precision gene therapy in ALS.</p>","PeriodicalId":93965,"journal":{"name":"Current neurovascular research","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149172164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of the COVID-19 Pandemic on the Prognosis and Emergency Treatment of Patients with Ischemic Stroke in Suzhou, China: A Multicenter Retrospective Study.","authors":"Guo Zhou, Rongguang Ge, Rui Wang, Jiaping Xu, Qin Fu, Shoujiang You, Yongjun Cao","doi":"10.2174/0115672026500840261002064327","DOIUrl":"https://doi.org/10.2174/0115672026500840261002064327","url":null,"abstract":"<p><strong>Introduction: </strong>The COVID-19 pandemic has disrupted stroke care globally. This study aimed to assess the impact of COVID-19 on the clinical characteristics, acute treatment, and outcomes of patients with acute ischemic stroke (AIS) in Suzhou, China.</p><p><strong>Methods: </strong>This study retrospectively analyzed 506 hospitalized AIS patients from four stroke centers between December 10, 2022, and January 20, 2023. Patients were grouped by COVID- 19 infection status and timing. Clinical data and outcomes were compared with a pre-pandemic cohort from the SUMMITS-II Study.</p><p><strong>Results: </strong>Among included AIS patients, 54.3% were COVID-19-positive. Infected patients had higher baseline NIHSS scores, elevated inflammatory markers, and more in-hospital complications. Intravenous thrombolysis rates increased slightly during the pandemic, despite longer prehospital delays. Emotional disorders were more frequent post-stroke. COVID-19 infection, particularly concurrent with stroke onset, was linked to worse outcomes at 90 days and 1 year.</p><p><strong>Discussion: </strong>The findings suggest that the COVID-19 pandemic significantly influenced the clinical characteristics and outcomes of patients with acute ischemic stroke in Suzhou. Patients with AIS with concomitant COVID-19 infection presented with a higher prevalence of vascular risk factors and elevated inflammatory and coagulation markers. Moreover, COVID-19 infection occurring within one week of stroke onset was associated with more severe neurological deficits and poorer short- and long-term prognosis, highlighting the potential role of COVID-19 in worsening stroke outcomes.</p><p><strong>Conclusion: </strong>The COVID-19 pandemic adversely affected stroke severity and prognosis. While in-hospital workflows were preserved, delayed presentation and increased systemic burden contributed to unfavorable stroke outcomes. Strengthening stroke care delivery and psychological support during public health crises is essential.</p>","PeriodicalId":93965,"journal":{"name":"Current neurovascular research","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2026-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149166952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Air Pollution and Neurovascular Health in Pakistan: An Emerging Public Health Crisis in South Asia - A Narrative Review.","authors":"Hamid Khan, Adeel Ahmed, Syed Shahab Ud Din Shah, Mubin Mustafa Kiyani, Sumaiyah Obaid, Mirza Obaid Baig, Kaleem Imdad, Shahid Bashir","doi":"10.2174/0115672026460820260929113419","DOIUrl":"https://doi.org/10.2174/0115672026460820260929113419","url":null,"abstract":"<p><p>Air pollution is an increasingly important public health concern in Pakistan, especially in rapidly urbanizing cities where concentrations of PM2.5, PM10, and other airborne toxicants frequently exceed recommended safety limits. Although the respiratory and cardiovascular consequences of air pollution are widely recognized, its contribution to neurovascular injury remains comparatively underrepresented in public health planning. This review synthesizes national and international evidence on the relationship between air pollution exposure and neurovascular outcomes, with particular emphasis on stroke-related mechanisms, cerebrovascular injury, and evidence gaps relevant to Pakistan and South Asia. Current evidence suggests that fine and ultrafine particulate matter may contribute to neurovascular damage through systemic inflammation, oxidative stress, endothelial dysfunction, blood-brain barrier disruption, microglial activation, vascular inflammation, atherosclerosis, and pro-thrombotic changes. These pathways provide biologically plausible links between chronic pollutant exposure and increased susceptibility to ischemic stroke, hemorrhagic stroke, cerebral small vessel disease, and impaired neurological recovery. However, Pakistan-specific longitudinal studies, biomarker-based investigations, and exposure-linked stroke surveillance data remain limited, restricting the integration of environmental exposure into neurovascular risk assessment and policy development. Given Pakistan's high pollution burden, dense urban populations, and increasing stroke-related morbidity, air pollution should be considered a potentially modifiable neurovascular risk factor. Strengthening air-quality monitoring, developing local epidemiological cohorts, integrating pollution exposure with hospital and stroke-registry data, and implementing targeted prevention strategies for high-risk populations may help reduce the future burden of pollution-associated neurovascular disease in Pakistan.</p>","PeriodicalId":93965,"journal":{"name":"Current neurovascular research","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2026-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149171640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Crossing the Blood-brain Barrier: Emerging Nanotechnological Approaches for Neurodegenerative Disease Therapy.","authors":"Alpana, Hitesh Kumar Dewangan","doi":"10.2174/0115672026454704261001071449","DOIUrl":"https://doi.org/10.2174/0115672026454704261001071449","url":null,"abstract":"<p><p>Neurodegenerative disorders such as Parkinson's Disease (PD), Alzheimer's Disease (AD), Amyotrophic Lateral Sclerosis (ALS), and Huntington's Disease (HD) are characterized by progressive neuronal degeneration and severe therapeutic limitations due to the Blood-Brain Barrier (BBB). Recent advances in nanotechnology have enabled the development of nanoscale drug delivery systems capable of improving BBB penetration and enhancing therapeutic efficacy. This review discusses recent progress in Lipid Nanoparticles (LNPs), polymeric nanoparticles, exosomes, magnetic nanoparticles, gold nanoparticles, graphene quantum dots, and RNAloaded nanocarriers for brain-targeted delivery. Special emphasis is placed on receptor-mediated transcytosis, intranasal delivery, magnetic targeting, and ionizable lipid nanoparticle systems for nucleic acid delivery. Recent nanoformulations including curcumin-loaded nanoparticles, siRNA- loaded lipid nanoparticles, dopamine-loaded liposomes, and lactoferrin-functionalized polymeric nanoparticles are critically compared based on BBB penetration, therapeutic efficacy, toxicity, and translational potential. Furthermore, current clinical challenges including nanotoxicity, pharmacokinetics, large-scale manufacturing, and regulatory barriers are discussed. Nanotechnology- based therapeutics represent a promising strategy for improving diagnosis and treatment of neurodegenerative disorders and may facilitate the future development of precision nanomedicine.</p>","PeriodicalId":93965,"journal":{"name":"Current neurovascular research","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2026-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149168921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic Hypothermia in Ischemic Stroke: Challenges and Pharmacological Opportunities.","authors":"Han Su, Haoxiao Chang, Jingyan Zhao","doi":"10.2174/0115672026523945260930110550","DOIUrl":"https://doi.org/10.2174/0115672026523945260930110550","url":null,"abstract":"","PeriodicalId":93965,"journal":{"name":"Current neurovascular research","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149167756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Cosmology of Stroke: A Systematic Review and Meta-analysis of the Lunar Influence on Cerebrovascular Disorders.","authors":"Yasser Aladdin","doi":"10.2174/0115672026477390260902113945","DOIUrl":"https://doi.org/10.2174/0115672026477390260902113945","url":null,"abstract":"<p><strong>Introduction: </strong>Measurable changes in blood pressure, coagulation, neurophysiological activity, and autonomic regulation were observed in relation to the lunar cycle. A few studies evaluated the circalunar rhythm of stroke in relation to synodic moon phases. Stroke represents an ongoing strain on the global economy as a leading cause of mortality and physical disability. This systematic review analyzed studies on the influence of the lunar cycle on cerebrovascular disorders.</p><p><strong>Methods: </strong>A systematic analysis of studies on the effects of various moon phases on stroke was conducted using both quantitative meta-analysis and qualitative appraisal of observational studies, following the Joanna Briggs Institute format for systematic reviews of prevalence studies, to ensure a comprehensive and rigorous evaluation of the existing evidence.</p><p><strong>Results: </strong>A total of 130556 patients from five studies were analyzed using qualitative and quantitative meta-analyses across all stroke types. Quantitative meta-analysis showed no association of the lunar cycle with ischemic or hemorrhagic strokes. However, the qualitative analyses yielded mixed and inconclusive results regarding the association between moon phase and the rates of ischemic or hemorrhagic stroke.</p><p><strong>Discussion: </strong>The current body of studies on lunar chronobiology in stroke is confined to smallscale, predominantly single-center, retrospective studies. The diversity of populations, the lack of uniform adjustments for comorbidities or medications, and substantial methodological heterogeneity preclude firm conclusions. The ancillary evidence of circalunar rhythm in blood pressure, autonomic regulation, platelet functions, and coagulation parameters suggests a lunar effect and warrants validation in large-scale studies.</p><p><strong>Conclusion: </strong>The limited evidence about the associations between stroke rates and the lunar cycle is mixed and inconclusive. Controlled studies spanning diverse geographic regions across the equator and multiple time zones are required to investigate the hypothetical moon effect on stroke rates. Identifying a lunar influence on stroke rates will guide critical econometric and chronotherapeutic strategies, such as dynamic dosing or drug titration, to address the circalunar biological rhythms for stroke prevention. The occult lunar rhythm on human tides may far exceed that of ocean tides, both biologically and economically.</p>","PeriodicalId":93965,"journal":{"name":"Current neurovascular research","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2026-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149139974","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astrocytic Multimodal Programmed Cell Death in Ischemic Stroke: Regulatory Mechanisms and Translational Prospects.","authors":"Li Zhang, Yonglan Ruan","doi":"10.2174/0115672026516896260924071212","DOIUrl":"https://doi.org/10.2174/0115672026516896260924071212","url":null,"abstract":"<p><strong>Introduction: </strong>Ischemic stroke remains a leading cause of disability and mortality worldwide. Current neuroprotective treatments predominantly target neurons and fail to address the complex post-ischemic cell death cascades in astrocytes, the most abundant glial cells in the central nervous system, whose multimodal Programmed Cell Death (PCD) directly determines blood-brain barrier integrity, neuroinflammation, and secondary brain injury.</p><p><strong>Methods: </strong>The literature on astrocytic PCD in ischemic stroke was systematically reviewed before April 2026, encompassing spatiotemporal dynamics, molecular mechanisms, inter-pathway crosstalk, and translational strategies in preclinical and clinical models.</p><p><strong>Results: </strong>Astrocytes undergo spatiotemporally regulated multimodal PCD apoptosis, necroptosis, pyroptosis, ferroptosis, and autophagic cell death with pronounced regional heterogeneity between ischemic core and penumbra. Single-cell transcriptomic analyses reveal distinct death subpopulations distributed in a brain-region-specific manner. Important molecular switches including iron metabolism, reactive oxygen species, RIPK1, and the p53/NF-κB axis integrate multiple death pathways into a hierarchical crosstalk network. Astrocytic death functions as an important amplifier governing neurovascular unit integrity.</p><p><strong>Discussion: </strong>A precision therapy strategy was proposed grounded in dominant astrocytic death subtypes, incorporating stage-specific targeting, nanotechnology-enabled drug delivery, and astrocyte reprogramming toward neuroprotective phenotypes. Translational challenges include interspecies differences, incomplete spatiotemporal molecular mapping, and absence of clinically validated biomarkers. Future integration of multiomics and humanized models is needed to bridge the preclinical-clinical gap.</p><p><strong>Conclusion: </strong>Astrocytic multimodal PCD provides novel mechanistic insights and translational targets for neurovascular protection after ischemic stroke, facilitating the paradigm shift from neurocentric neuroprotection to neuron-glia synergistic therapy.</p>","PeriodicalId":93965,"journal":{"name":"Current neurovascular research","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149120837","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unravelling Anti-parkinson's Potential of Combined Extracts of Juglans regia L. and Cardiospermum halicacabum L. through an in silico Approach.","authors":"Himangi Vig, Anuradha Mishra, Ankita Wal","doi":"10.2174/0115672026498637260915061239","DOIUrl":"https://doi.org/10.2174/0115672026498637260915061239","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Introduction: &lt;/strong&gt;Dopaminergic neuronal loss, mitochondrial dysfunction, oxidative stress, and neurotransmitter imbalance are the hallmarks of Parkinson's Disease (PD), a progressive neurodegenerative disorder. Despite their established antioxidant and neuroprotective qualities, the mechanistic significance of Juglans regia L. and Cardiospermum halicacabum L. in Parkinson's disease remains unclear, especially in the context of extract-based treatment approaches.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;Drug-likeness and ADMET properties were evaluated with SwissADME and ADMETlab 3.0, respectively. SwissTargetPrediction was used to predict potential targets of selected phytoconstituents, whereas gene sets associated with Parkinson's disease were mined from Dis- GeNET and GeneCards. Venn analysis was performed to identify overlapping targets for drugs, followed by Protein-Protein Interaction (PPI) network construction using STRING and topological analysis in Cytoscape. Gene Ontology (GO) and KEGG pathway enrichment analysis were performed using DAVID 2021, then a Bioactive Compound-Target-Pathway (BA-TAR-PATH) network was constructed. Molecular docking based on AutoDock Vina was used to predict the binding affinity between the protein and ligand for the top 10 hits; then, molecular dynamics simulation using GROMACS was applied to assess the stability of the protein-ligand complexes.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Result: &lt;/strong&gt;Phytochemical characterization by HPTLC, FTIR, HPLC, and ESI-MS supported the presence of flavonoids, phenolic compounds, tannins, and lipid-associated constituents in the combined extract. Target prediction yielded 355 related compounds and 30 PD-associated genes, identifying five overlapping targets (ACHE, DRD2, MAOB, COMT, and SLC6A3). Molecular docking revealed favourable binding interactions, particularly quercetin-ACHE (-11.4 kcal/mol), while molecular dynamics simulations supported the stability of selected protein-ligand complexes.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Discussion: &lt;/strong&gt;Network analysis highlighted MAOB, COMT, and SLC6A3 as key hub genes. GO and KEGG analyses revealed significant enrichment of dopaminergic synapse, neuroactive ligand- receptor signalling, and Parkinson disease pathways. Molecular docking demonstrated stable binding interactions, notably quercetin-ACHE (-11.4 kcal/mol), supporting the therapeutic relevance of flavonoids.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;Based on the above findings, we propose that both J. regia kernel and C. halicacabum seed extracts may contain phytoconstituents that interact with various PD-related targets and pathways linked to dopaminergic neurotransmission and oxidative stress. This extractanchored network pharmacology approach presents a mechanism-related framework to facilitate follow-up experiments targeting specific bioactive constituents and molecular targets. At the same time, the results come exclusively from computational analyses and should be treated as hypothesis-generating. In ","PeriodicalId":93965,"journal":{"name":"Current neurovascular research","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149120589","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in the Mechanisms Underlying Brain Injury after Resuscitation from Cardiac Arrest.","authors":"Wenxun Liu, Xiaohong Zhou, Wusheng Liu, Jiaxiang Ren, Wenjuan Zhang","doi":"10.2174/0115672026504763260924073702","DOIUrl":"https://doi.org/10.2174/0115672026504763260924073702","url":null,"abstract":"<p><strong>Introduction: </strong>Cardiac arrest (CA) causes global cerebral ischemia. Secondary reperfusion injury frequently worsens neurological dysfunction, making cerebral resuscitation more difficult, even when cardiopulmonary resuscitation (CPR) helps restore spontaneous circulation (ROSC). With an emphasis on early primary ischemic injury and the ensuing reperfusionassociated pathological cascade, this review clarifies the pathophysiological processes of brain injury after CA-CPR.</p><p><strong>Methods: </strong>This study reviewed the literature on cerebral pathophysiology following CA-CPR, focusing on studies that explore the mechanisms underlying ischemia, hypoxia, and reperfusion injury. Relevant peer-reviewed articles published between 2016 and 2026 were extracted through searches of PubMed, Embase, and Web of Science. The search keywords included \"cardiac arrest,\" \"global cerebral ischemia,\" \"four-vessel occlusion,\" \"asphyxia-induced cardiac arrest,\" \"reperfusion injury,\" and \"neuroprotection.\" Studies published within the past 5 years were prioritized to reflect recent advancements.</p><p><strong>Results: </strong>Multiple interconnected pathways contribute to brain injury, following a distinct temporal sequence from primary ischemic depolarization to secondary reperfusion-induced dysregulation. These include energy metabolism disorders, excitotoxicity, calcium overload, mitochondrial dysfunction, oxidative stress, and neuroinflammation. Furthermore, major neuroprotective strategies are evaluated for their efficacy in mitigating secondary injury.</p><p><strong>Discussion: </strong>Cerebral resuscitation is particularly difficult owing to the interplay among these complex mechanisms. Consequently, targeting multiple pathways simultaneously may be more effective than focusing on a single one.</p><p><strong>Conclusion: </strong>Brain injury after CA-CPR involves multifactorial pathophysiological processes. Elucidating these mechanisms will establish a groundwork for the development of neuroprotective strategies. However, further research is warranted to translate these findings into clinical practice.</p>","PeriodicalId":93965,"journal":{"name":"Current neurovascular research","volume":" ","pages":""},"PeriodicalIF":1.7,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149120867","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}