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Prog Neurobiol. 2014 Apr;115:138-56. doi: 10.1016/j.pneurobio.2013.11.004. Epub 2013 Nov 27.

Vascular remodeling after ischemic stroke: mechanisms and therapeutic potentials.

Author information

1
Department of Neurological Surgery, UCSF, San Francisco, CA 94121, USA; SFVAMC, San Francisco, CA 94121, USA. Electronic address: jialing.liu@ucsf.edu.
2
Neuroscience and Neuroengineering Research Center, Med-X Research Institute, Shanghai 200030, China; School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China; Department of Neurology, Shanghai Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200025, China.
3
Department of Neurological Surgery, UCSF, San Francisco, CA 94121, USA; SFVAMC, San Francisco, CA 94121, USA; Department of Neurological Surgery, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai 980-8574, Japan.
4
Department of Neurological Surgery, UCSF, San Francisco, CA 94121, USA; SFVAMC, San Francisco, CA 94121, USA.
5
Center of Cerebrovascular Disease Research, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.
6
Department of Neurological Surgery, UCSF, San Francisco, CA 94121, USA.
7
Neuroscience and Neuroengineering Research Center, Med-X Research Institute, Shanghai 200030, China; School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai 200030, China; Department of Neurology, Shanghai Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200025, China. Electronic address: gyyang0626@gmail.com.

Abstract

The brain vasculature has been increasingly recognized as a key player that directs brain development, regulates homeostasis, and contributes to pathological processes. Following ischemic stroke, the reduction of blood flow elicits a cascade of changes and leads to vascular remodeling. However, the temporal profile of vascular changes after stroke is not well understood. Growing evidence suggests that the early phase of cerebral blood volume (CBV) increase is likely due to the improvement in collateral flow, also known as arteriogenesis, whereas the late phase of CBV increase is attributed to the surge of angiogenesis. Arteriogenesis is triggered by shear fluid stress followed by activation of endothelium and inflammatory processes, while angiogenesis induces a number of pro-angiogenic factors and circulating endothelial progenitor cells (EPCs). The status of collaterals in acute stroke has been shown to have several prognostic implications, while the causal relationship between angiogenesis and improved functional recovery has yet to be established in patients. A number of interventions aimed at enhancing cerebral blood flow including increasing collateral recruitment are under clinical investigation. Transplantation of EPCs to improve angiogenesis is also underway. Knowledge in the underlying physiological mechanisms for improved arteriogenesis and angiogenesis shall lead to more effective therapies for ischemic stroke.

KEYWORDS:

Angiogenesis; Arteriogenesis; Collateral flow; Fluid shear stress; Macrophage polarization; Pro-angiogenic factors

PMID:
24291532
PMCID:
PMC4295834
DOI:
10.1016/j.pneurobio.2013.11.004
[Indexed for MEDLINE]
Free PMC Article

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