Mechanical thrombectomy has reshaped the management of acute ischemic stroke, offering rapid recanalization and improved neurological outcomes. However, emerging clinical observations suggest that vascular alterations following thrombectomy particularly endothelial injury, hemodynamic stress redistribution, and inflammatory cascades may predispose certain patients to delayed vascular complications, including de novo or progressive aneurysm formation. These post-thrombectomy vascular changes remain insufficiently characterized, both mechanistically and clinically.
In parallel, glioblastoma continues to represent the most aggressive primary brain tumor, marked by profound vascular dysregulation, aberrant angiogenesis, and a highly adaptive microenvironment. Increasing attention has been directed toward the role of cerebrovascular dynamics in influencing tumor growth, invasion patterns, and therapeutic resistance.
Despite being traditionally studied as distinct entities, there is a growing conceptual intersection between post-stroke vascular remodeling and tumor biology. Shared pathways including endothelial dysfunction, hypoxia-driven signaling, extracellular matrix remodeling, and immune activation suggest that cerebrovascular injury and tumor progression may not be independent processes. Notably, the impact of prior ischemic events or endovascular interventions on glioblastoma behavior remains largely unexplored.
This Research Topic aims to bring together multidisciplinary insights from vascular neurology, interventional neuroradiology, and neuro-oncology to explore the continuum between thrombectomy-induced vascular changes, aneurysm development, and glioblastoma progression.
This Research Topic also seeks to: - Elucidate the mechanisms underlying vascular remodeling following mechanical thrombectomy - Characterize the incidence, predictors, and clinical relevance of post-thrombectomy aneurysm formation - Investigate the influence of altered cerebral hemodynamics on tumor initiation and progression - Explore shared molecular pathways between ischemic injury and glioblastoma angiogenesis - Evaluate the impact of prior stroke or endovascular therapy on glioblastoma outcomes - Identify potential therapeutic targets at the interface of vascular repair and tumor control
Submissions may include, but are not limited to: - Endothelial injury and repair mechanisms after thrombectomy - Hemodynamic stress and delayed aneurysm formation - Neuroinflammation and its role in vascular and tumour remodelling - Hypoxia-inducible pathways linking ischemia and tumor growth - Angiogenesis and vascular mimicry in glioblastoma - Imaging biomarkers of vascular instability post-intervention - Clinical studies on stroke history and glioblastoma prognosis - Experimental models exploring stroke–tumor interactions - Advances in endovascular techniques and their long-term vascular effects - Translational approaches targeting vascular–tumor crosstalk.
By integrating cerebrovascular intervention with oncological progression, this Research Topic addresses an underexplored but clinically relevant interface. A deeper understanding of how post-thrombectomy vascular alterations influence aneurysm formation and tumor biology could redefine surveillance strategies, risk stratification, and therapeutic approaches in both stroke survivors and neuro-oncology patients.
This collection will be of interest to neurologists, neurosurgeons, interventional neuroradiologists, neuro-oncologists, vascular biologists, and translational researchers working at the intersection of cerebrovascular disease and brain tumors.
Please note: Manuscripts consisting solely of bioinformatics, computational analysis, or predictions of public databases which are not accompanied by validation (independent clinical or patient cohort, or biological validation in vitro or in vivo, which are not based on public databases) are not suitable for publication in this journal.
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