Extracellular Vesicles: Biology, Mechanisms, and Therapies for Cerebrovascular Disorders

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Physiology and Pathology".

Deadline for manuscript submissions: 30 June 2026 | Viewed by 592

Special Issue Editor


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Guest Editor
Department of Biomedical Sciences, Joan C Edwards School of Medicine, Marshall University, Huntington, WV 25755, USA
Interests: extracellular vesicles; microRNAs; stroke; vascular cognitive impairment and dementia; aging; hypertension; exercise; neuroinflammation; angiogenesis; neurogenesis
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Special Issue Information

Dear Colleagues,

Extracellular vesicles (EVs) are emerging as vital mediators of intercellular communication across a wide spectrum of physiological and pathological processes. Once considered cellular waste carriers, EVs are now recognized as active conveyors of bioactive molecules such as RNAs, proteins, lipids, and metabolites. Their ability to cross biological barriers, particularly the blood-brain barrier, has generated tremendous interest in their roles within the central nervous system and their potential as diagnostic biomarkers and therapeutic delivery vehicles.

Increasing evidence suggest that dysregulation of EV cargo and trafficking contributes to the pathogenesis of cerebrovascular diseases. Furthermore, engineered EVs and EV-mimetic systems have shown promise as innovative therapeutic platforms for targeted drug delivery, gene regulation, and tissue repair. Despite this progress, key challenges remain, such as limited understanding of their biodistribution and targeting mechanisms for clinical application.

The scope of this special issue is to bring together recent advances and challenges in EV biology, engineering, and translational applications, with a particular emphasis on cerebrovascular diseases. We invite original research articles, reviews, and perspectives that advance our understanding of mechanistic, diagnostic, and therapeutic dimensions of EVs in the context of cerebrovascular disorders, including stroke, vascular cognitive impairment and dementia, aneurysms, arteriovenous malformation, cerebral small vessel diseases, cerebral amyloid angiopathy, etc. Submissions covering cross-disciplinary themes, such as biomaterials, nanomedicine, or computational analysis, are also encouraged.

Dr. Jinju Wang
Guest Editor

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Keywords

  • extracellular vesicles
  • cerebrovascular disorders
  • dementia
  • extracellular vesicle-based therapy

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Published Papers (1 paper)

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Research

17 pages, 7147 KB  
Article
Exercise-Conditioned Endothelial Progenitor Cell-Exosomes Preserve Cerebral Blood Flow and Alleviate Acute Ischemic Brain Injury in Hypertensive Mice
by Shuzhen Chen, Smara Sigdel, Gideon Udoh, Brandon Xiang Yu and Jinju Wang
Life 2026, 16(4), 623; https://doi.org/10.3390/life16040623 - 8 Apr 2026
Viewed by 383
Abstract
Exosomes (EXs) mediate intercellular communication in the tissue microenvironment. We previously demonstrated that endothelial progenitor cell-derived exosomes (EPC-EXs) from exercised mice protect neurons and cerebral endothelial cells from hypoxia- and hypertension- induced injury ex vivo, suggesting their therapeutic potential in hypertensive ischemic injury. [...] Read more.
Exosomes (EXs) mediate intercellular communication in the tissue microenvironment. We previously demonstrated that endothelial progenitor cell-derived exosomes (EPC-EXs) from exercised mice protect neurons and cerebral endothelial cells from hypoxia- and hypertension- induced injury ex vivo, suggesting their therapeutic potential in hypertensive ischemic injury. Here, we investigated whether exercise-conditioned EPC-EXs (ET-EPC-EXs) confer protection against acute ischemic injury. Hypertensive transgenic mice were divided into donor and recipient groups. Donor mice underwent treadmill exercise to generate ET-EPC-EXs. Recipient mice was subjected to middle cerebral artery occlusion and received ET-EPC-EXs via tail vein injection (2 × 108/100 μL saline) two hours after stroke onset. Cerebral blood flow (CBF) was assessed, and brains were collected on day two for histological and molecular analyses. Our data showed that ET-EPC-EXs were robustly taken up by cerebral cells, predominantly in the penumbra in the ipsilateral hemisphere. ET-EPC-EXs reduced cell death and microglia activation and restored tight-junction proteins. Moreover, ET-EPC-EX treatment preserved CBF and improved sensorimotor function on day two post-stroke. Mechanistically, ET-EPC-EXs suppressed p38 activation, accompanied by reduced matrix metalloproteinase-3 and cytochrome c levels in the ipsilateral brain. Collectively, these findings demonstrate that EPC-EXs from exercise mice improve sensorimotor functions and confer protection in hypertensive ischemic brain injury, likely through attenuation of neuroinflammation and preservation of vascular integrity via modulation of the p38 signaling. Full article
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