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Review
. 2022 Mar 4:16:860573.
doi: 10.3389/fncel.2022.860573. eCollection 2022.

Neuroprotective Effect of Physical Activity in Ischemic Stroke: Focus on the Neurovascular Unit

Affiliations
Review

Neuroprotective Effect of Physical Activity in Ischemic Stroke: Focus on the Neurovascular Unit

Hui Zhang et al. Front Cell Neurosci. .

Abstract

Cerebral ischemia is one of the major diseases associated with death or disability among patients. To date, there is a lack of effective treatments, with the exception of thrombolytic therapy that can be administered during the acute phase of ischemic stroke. Cerebral ischemia can cause a variety of pathological changes, including microvascular basal membrane matrix, endothelial cell activation, and astrocyte adhesion, which may affect signal transduction between the microvessels and neurons. Therefore, researchers put forward the concept of neurovascular unit, including neurons, axons, astrocytes, microvasculature (including endothelial cells, basal membrane matrix, and pericyte), and oligodendrocytes. Numerous studies have demonstrated that exercise can produce protective effects in cerebral ischemia, and that exercise may protect the integrity of the blood-brain barrier, promote neovascularization, reduce neuronal apoptosis, and eventually lead to an improvement in neurological function after cerebral ischemia. In this review, we summarized the potential mechanisms on the effect of exercise on cerebral ischemia, by mainly focusing on the neurovascular unit, with the aim of providing a novel therapeutic strategy for future treatment of cerebral ischemia.

Keywords: blood-brain barrier; cerebral ischemia; exercise; mechanism; neurovascular unit.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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References

    1. Abdullahi W., Tripathi D., Ronaldson P. T. (2018). Blood-brain barrier dysfunction in ischemic stroke: targeting tight junctions and transporters for vascular protection. Am. J. Physiol. Cell Physiol. 315 C343–C356. 10.1152/ajpcell.00095.2018 - DOI - PMC - PubMed
    1. Al Ahmad A., Taboada C. B., Gassmann M., Ogunshola O. O. (2011). Astrocytes and pericytes differentially modulate blood-brain barrier characteristics during development and hypoxic insult. J. Cereb. Blood Flow Metab. 31 693–705. 10.1038/jcbfm.2010.148 - DOI - PMC - PubMed
    1. Arrick D. M., Sun H., Mayhan W. G. (2012). Influence of exercise training on ischemic brain injury in type 1 diabetic rats. J. Appl. Physiol. (1985). 113 1121–1127. 10.1152/japplphysiol.00437.2012 - DOI - PMC - PubMed
    1. Barde Y. A., Edgar D., Thoenen H. (1982). Purification of a new neurotrophic factor from mammalian brain. Embo J. 1 549–553. 10.1002/j.1460-2075.1982.tb01207.x - DOI - PMC - PubMed
    1. Barr L. A., Lambert J. P., Shimizu Y., Barouch L. A., Naqvi N., Calvert J. W. (2017). Exercise training provides cardioprotection by activating and coupling endothelial nitric oxide synthase via a β(3)-adrenergic receptor-AMP-activated protein kinase signaling pathway. Med. Gas Res. 7 1–8. 10.4103/2045-9912.202904 - DOI - PMC - PubMed

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