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Trophic factors and cell therapy to stimulate brain repair after ischaemic stroke.

Gutiérrez-Fernández M, Fuentes B, Rodríguez-Frutos B, Ramos-Cejudo J, Vallejo-Cremades MT, Díez-Tejedor E - J. Cell. Mol. Med. (2012)

Bottom Line: From a therapeutic viewpoint, reparative therapies that encourage cerebral plasticity are needed.However, even when promising results have been obtained in a wide range of experimental animal models and conditions these preliminary results have not yet demonstrated their clinical efficacy.Here, we focus on brain repair modulatory treatments for ischaemic stroke, that use trophic factors, drugs with trophic effects and stem cell therapy.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology and Stroke Centre, La Paz University Hospital, Neuroscience Area of IdiPAZ (Health Research Institute), Autónoma University of Madrid, Madrid, Spain.

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Pathogenic mechanisms and therapeutic options in cerebral infarct. Time line for the mechanisms and therapy involved in endogenous protection and brain protection-repair after ischaemic stroke. MSCs: mesenchymal stem cells; UCBCs: umbilical cord blood cells; DSCs: dental stem cells; ESCs: embryonic stem cells; BMSCs: bone marrow stem cells; NSCs: neural stem cells; G-CSF: granulocyte colony-stimulating factor; VEGF: vascular endothelial growth factor; BDNF: brain-derived neurotrophic factor; NGF: nerve growth factor; bFGF: basic fibroblast growth factor; IGF-1: insulin growth factor-1; EPO: erythropoietin.
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fig01: Pathogenic mechanisms and therapeutic options in cerebral infarct. Time line for the mechanisms and therapy involved in endogenous protection and brain protection-repair after ischaemic stroke. MSCs: mesenchymal stem cells; UCBCs: umbilical cord blood cells; DSCs: dental stem cells; ESCs: embryonic stem cells; BMSCs: bone marrow stem cells; NSCs: neural stem cells; G-CSF: granulocyte colony-stimulating factor; VEGF: vascular endothelial growth factor; BDNF: brain-derived neurotrophic factor; NGF: nerve growth factor; bFGF: basic fibroblast growth factor; IGF-1: insulin growth factor-1; EPO: erythropoietin.

Mentions: We should first consider that protection and repair mechanisms are activated and work together from the very beginning of cerebral ischaemia (Fig. 1). The accompanying hypoxia and glucose deprivation, cell death programs and immunological events of ischaemia are initiated to remove damaged cells and tissue debris and to prepare injured areas for repair processes [6–8] and as a response to injury, transcriptional programs associated with axonal sprouting, survival and myelin formation are activated and maintained from the very beginning [9, 10]. Research is now focused on how to modulate these processes to preserve all the structures that make up the neurovascular unit, including microvessels and pericytes (vascular protection), neurons and their axons (neuroprotection), astrocytes and other supportive cells such as oligodendroglia [11].


Trophic factors and cell therapy to stimulate brain repair after ischaemic stroke.

Gutiérrez-Fernández M, Fuentes B, Rodríguez-Frutos B, Ramos-Cejudo J, Vallejo-Cremades MT, Díez-Tejedor E - J. Cell. Mol. Med. (2012)

Pathogenic mechanisms and therapeutic options in cerebral infarct. Time line for the mechanisms and therapy involved in endogenous protection and brain protection-repair after ischaemic stroke. MSCs: mesenchymal stem cells; UCBCs: umbilical cord blood cells; DSCs: dental stem cells; ESCs: embryonic stem cells; BMSCs: bone marrow stem cells; NSCs: neural stem cells; G-CSF: granulocyte colony-stimulating factor; VEGF: vascular endothelial growth factor; BDNF: brain-derived neurotrophic factor; NGF: nerve growth factor; bFGF: basic fibroblast growth factor; IGF-1: insulin growth factor-1; EPO: erythropoietin.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3823421&req=5

fig01: Pathogenic mechanisms and therapeutic options in cerebral infarct. Time line for the mechanisms and therapy involved in endogenous protection and brain protection-repair after ischaemic stroke. MSCs: mesenchymal stem cells; UCBCs: umbilical cord blood cells; DSCs: dental stem cells; ESCs: embryonic stem cells; BMSCs: bone marrow stem cells; NSCs: neural stem cells; G-CSF: granulocyte colony-stimulating factor; VEGF: vascular endothelial growth factor; BDNF: brain-derived neurotrophic factor; NGF: nerve growth factor; bFGF: basic fibroblast growth factor; IGF-1: insulin growth factor-1; EPO: erythropoietin.
Mentions: We should first consider that protection and repair mechanisms are activated and work together from the very beginning of cerebral ischaemia (Fig. 1). The accompanying hypoxia and glucose deprivation, cell death programs and immunological events of ischaemia are initiated to remove damaged cells and tissue debris and to prepare injured areas for repair processes [6–8] and as a response to injury, transcriptional programs associated with axonal sprouting, survival and myelin formation are activated and maintained from the very beginning [9, 10]. Research is now focused on how to modulate these processes to preserve all the structures that make up the neurovascular unit, including microvessels and pericytes (vascular protection), neurons and their axons (neuroprotection), astrocytes and other supportive cells such as oligodendroglia [11].

Bottom Line: From a therapeutic viewpoint, reparative therapies that encourage cerebral plasticity are needed.However, even when promising results have been obtained in a wide range of experimental animal models and conditions these preliminary results have not yet demonstrated their clinical efficacy.Here, we focus on brain repair modulatory treatments for ischaemic stroke, that use trophic factors, drugs with trophic effects and stem cell therapy.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology and Stroke Centre, La Paz University Hospital, Neuroscience Area of IdiPAZ (Health Research Institute), Autónoma University of Madrid, Madrid, Spain.

Show MeSH
Related in: MedlinePlus