title: [Reorganisation of the cerebral vasculature following ischaemia].
abstract: BACKGROUND
  Cerebral function needs a constant oxygen and glucose supply. This is why the regulation of cerebral blood flow is critical for the maintenance of neuronal function. Therefore, vascular system in adult brain is extremely stable and does not withstand big changes under physiological conditions. However, when blood flow is interrupted due to a focal cerebral ischemia the collateral tissue is partially affected, this is known as ischemic penumbra. Although its functionality is affected, this tissue is viable thanks to the collateral blood flow, and it releases angiogenic factors that induce proliferation of endothelial cells and migration of endothelial progenitor cells for the formation of new blood vessels. Angiogenesis induction and new vessel generation allow neurorepair processes, including neurogenesis and synaptogenesis. These two processes should be coupled with angiogenesis in order to contribute to functional recovery of patients who suffered a cerebral infarct. Therefore, angiogenesis could be one of the therapeutic options in ischemic stroke treatment. Nevertheless, some angiogenic factors such as vascular endothelial growth factor, platelet derived growth factor and angiopoyetin also increase vascular permeability which can produce hemorrhagic transformation.
  
  
  CONCLUSIONS
  Hence, the knowledge of molecular mechanisms that regulate angiogenesis after an ischemic stroke could contribute to the development of a new therapeutic option based on angiogenesis as a vehicle to promote neurorepair and functional recovery.
authors.affiliation: Laboratorio de Investigación de Neurociencias Clínicas, Servicio de Neurología, Hospital Clinico de Santiago de Compostela, E-15706 Santiago de Compostela (A Coruña), Espana.
authors.forename: D
authors.initials: D
authors.lastname: Brea
authors.forename: T
authors.initials: T
authors.lastname: Sobrino
authors.forename: P
authors.initials: P
authors.lastname: Ramos-Cabrer
authors.forename: J
authors.initials: J
authors.lastname: Castillo
mesh_terms: D015415:Biomarkers / Q000378:metabolism; D001921:Brain / Q000098:blood supply / Q000502:physiology; D002545:Brain Ischemia / Q000473:pathology* / Q000503:physiopathology* / Q000628:therapy; D002454:Cell Differentiation / Q000502:physiology; D002465:Cell Movement / Q000502:physiology; D064987:Cell- and Tissue-Based Therapy; D002560:Cerebrovascular Circulation; D003097:Collateral Circulation / Q000502:physiology; D042783:Endothelial Cells / Q000502:physiology; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins / Q000378:metabolism; D018919:Neovascularization, Physiologic / Q000502:physiology*; D017978:Receptors, Growth Factor / Q000378:metabolism; D020127:Recovery of Function; D013234:Stem Cells / Q000502:physiology; D016212:Transforming Growth Factor beta / Q000378:metabolism
chemical_list: D015415:Biomarkers; D036341:Intercellular Signaling Peptides and Proteins; D017978:Receptors, Growth Factor; D016212:Transforming Growth Factor beta