Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2011 Sep;26(9):1193-8.
doi: 10.1177/0883073811408610. Epub 2011 May 31.

Cellular mechanisms of neurovascular damage and repair after stroke

Affiliations
Review

Cellular mechanisms of neurovascular damage and repair after stroke

Ken Arai et al. J Child Neurol. 2011 Sep.

Abstract

The biological processes underlying stroke are complex, and patients have a narrow repertoire of therapeutic opportunities. After the National Institutes of Health (NIH) convened the Stroke Progress Review Group in 2001, stroke research shifted from having a purely neurocentric focus to adopting a more integrated view wherein dynamic interactions between all cell types contribute to function and dysfunction in the brain. This so-called "neurovascular unit" provides a conceptual framework that emphasizes cell-cell interactions between neuronal, glial, and vascular elements. Under normal conditions, signaling within the neurovascular unit helps maintain homeostasis. After stroke, cell-cell signaling is disturbed, leading to pathophysiology. More recently, emerging data now suggest that these cell-cell signaling mechanisms may also mediate parallel processes of neurovascular remodeling during stroke recovery. Because plasticity is a signature feature of the young and developing brain, these concepts may have special relevance to how the pediatric brain responds after stroke.

PubMed Disclaimer

Figures

Figure 1
Figure 1
In central core areas of stroke, blood flow deficits and/or hemorrhagic lesions are severe and brain cells die rapidly. In peripheral areas (the penumbra), it has been proposed that cell death, inflammation and neurovascular perturbations proceed at a slower pace. Hence, therapeutic salvage is theoretically possible.
Figure 2
Figure 2
Trends in neurovascular unit research compiled from publications between 2001 and 2010. An online PubMed search based on the terms “neurovascular unit AND (stroke OR cerebral ischemia OR cerebral hemorrhage)” demonstrated a rapid growth of stroke-related neurovascular unit articles over the past 5 years. The PubMed search based on the terms “neurovascular unit AND (alzheimer OR parkinson OR dementia OR multiple sclerosis OR huntington OR amyotrophic lateral sclerosis OR moyamoya)” suggested that this concept is gradually applying to other CNS disorders.

Similar articles

Cited by

References

    1. Arai K, Jin G, Navaratna D, Lo EH. Brain angiogenesis in developmental and pathological processes: neurovascular injury and angiogenic recovery after stroke. FEBS J. 2009 Sep;276(17):4644–4652. - PMC - PubMed
    1. Lok J, Gupta P, Guo S, et al. Cell-cell signaling in the neurovascular unit. Neurochem Res. 2007 Dec;32(12):2032–2045. - PubMed
    1. Lo EH, Dalkara T, Moskowitz MA. Mechanisms, challenges and opportunities in stroke. Nat Rev Neurosci. 2003 May;4(5):399–415. - PubMed
    1. Moskowitz MA, Lo EH, Iadecola C. The science of stroke: mechanisms in search of treatments. Neuron. 2010 Jul 29;67(2):181–198. - PMC - PubMed
    1. Lo EH, Moskowitz MA, Jacobs TP. Exciting, radical, suicidal: how brain cells die after stroke. Stroke. 2005 Feb;36(2):189–192. - PubMed

Publication types

  NODES
twitter 2