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The Role of Pericytes in Neurovascular Unit Remodeling in Brain Disorders

Journal

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 15, Issue 4, Pages 6453-6474

Publisher

MDPI
DOI: 10.3390/ijms15046453

Keywords

pericytes; neurovascular unit; tissue remodeling; tissue repair; signal transduction; Alzheimer's disease; stroke

Funding

  1. Canadian Institutes of Health Research
  2. Multiple Sclerosis Scientific Research Foundation of Canada
  3. Canadian Stroke Network
  4. Canadian Stroke Network and European Stroke Network Collaborative Research Initiative, NORAMPAC' Alzheimer foundation
  5. Centre de Recherche en Endocrinologie Moleculaire et Oncologique et Genomique Humaine (CREMOGH)

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Neurons are extremely vulnerable cells that tightly rely on the brain's highly dynamic and complex vascular network that assures an accurate and adequate distribution of nutrients and oxygen. The neurovascular unit (NVU) couples neuronal activity to vascular function, controls brain homeostasis, and maintains an optimal brain microenvironment adequate for neuronal survival by adjusting blood-brain barrier (BBB) parameters based on brain needs. The NVU is a heterogeneous structure constituted by different cell types that includes pericytes. Pericytes are localized at the abluminal side of brain microvessels and contribute to NVU function. Pericytes play essential roles in the development and maturation of the neurovascular system during embryogenesis and stability during adulthood. Initially, pericytes were described as contractile cells involved in controlling neurovascular tone. However, recent reports have shown that pericytes dynamically respond to stress induced by injury upon brain diseases, by chemically and physically communicating with neighboring cells, by their immune properties and by their potential pluripotent nature within the neurovascular niche. As such, in this paper, we would like to review the role of pericytes in NVU remodeling, and their potential as targets for NVU repair strategies and consequently neuroprotection in two pathophysiologically distinct brain disorders: ischemic stroke and Alzheimer's disease (AD).

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