Effects of atorvastatin in the regulation of circulating EPCs and angiogenesis in traumatic brain injury in rats

Wang, Bin; Sun, Lin; Tian, Ye; Li, Zhanying; Wei, Huijie; Wang, Dong; Yang, Zhuo; Chen, Jieli; Zhang, Jianning; Jiang, Rongcai

doi:10.1016/j.jns.2012.04.015

Cited by 59 publications

(33 citation statements)

References 39 publications

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“…Other FDA-approved medications have proven beneficial in preclinical trials potentially through angiogenesis promotion after TCVI, including atorvastatin (Wang et al, 2012) and glibenclamide (Kurland et al, 2013). Both drugs have multiple modes of action.…”

Section: Preclinical Work With Treatments That Increase Cbf and Angiomentioning

confidence: 99%

Cerebral Vascular Injury in Traumatic Brain Injury

Kenney

Amyot

Haber

et al. 2016

Experimental Neurology

223

176

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Traumatic cerebral vascular injury (TCVI) is a very frequent, if not universal, feature after traumatic brain injury (TBI). It is likely responsible, at least in part, for functional deficits and TBI-related chronic disability. Because there are multiple pharmacologic and non-pharmacologic therapies that promote vascular health, TCVI is an attractive target for therapeutic intervention after TBI. The cerebral microvasculature is a component of the neurovascular unit (NVU) coupling neuronal metabolism with local cerebral blood flow. The NVU participates in the pathogenesis of TBI, either directly from physical trauma or as part of the cascade of secondary injury that occurs after TBI. Pathologically, there is extensive cerebral microvascular injury in humans and experimental animal, identified with either conventional light microscopy or ultrastructural examination. It is seen in acute and chronic TBI, and even described in chronic traumatic encephalopathy (CTE). Non-invasive, physiologic measures of cerebral microvascular function show dysfunction after TBI in humans and experimental animal models of TBI. These include imaging sequences (MRI-ASL), Transcranial Doppler (TCD), and Near InfraRed Spectroscopy (NIRS). Understanding the pathophysiology of TCVI, a relatively under-studied component of TBI, has promise for the development of novel therapies for TBI.

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Section: Preclinical Work With Treatments That Increase Cbf and Angiomentioning

confidence: 99%

Cerebral Vascular Injury in Traumatic Brain Injury

Kenney

Amyot

Haber

et al. 2016

Experimental Neurology

223

176

View full text Add to dashboard Cite

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“…Increased EPC circulation and vessel healing have been found by administering treatments such as atorvastatins 48 and erythropoietins. 49,50 Providing an exogenous erythropoietin delivery to mice to improve transplanted EPC survival to treat myocardial infarctions was found to be effective.…”

Section: External Treatmentsmentioning

confidence: 99%

Strategies and Techniques to Enhance theIn SituEndothelialization of Small-Diameter Biodegradable Polymeric Vascular Grafts

Melchiorri

Hibino

Fisher

2013

Tissue Engineering Part B: Reviews

154

147

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“…Vitamin D3 promotes angiogenesis in endothelial cell cultures [238]. Atorvastatin, pravastatin and simvastatin have both anti-and pro-angiogenic activities depending on the dose, specific angiogenic stimulus, and angiogenesis mechanism in the specific disease local microenviroment [239,240]. They have been tested as neurorepair attempts in several randomized clinical trials in combination with IFN-β and GA [241][242][243][244].…”

Section: Therapeutic Potential Of Targeting Angiogenesismentioning

confidence: 99%

Angiogenesis in multiple sclerosis and experimental autoimmune encephalomyelitis

Girolamo

Coppola

Ribatti

et al. 2014

Acta Neuropathologica Communications

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Angiogenesis, the formation of new vessels, is found in Multiple Sclerosis (MS) demyelinating lesions following Vascular Endothelial Growth Factor (VEGF) release and the production of several other angiogenic molecules. The increased energy demand of inflammatory cuffs and damaged neural cells explains the strong angiogenic response in plaques and surrounding white matter. An angiogenic response has also been documented in an experimental model of MS, experimental allergic encephalomyelitis (EAE), where blood-brain barrier disruption and vascular remodelling appeared in a pre-symptomatic disease phase. In both MS and EAE, VEGF acts as a pro-inflammatory factor in the early phase but its reduced responsivity in the late phase can disrupt neuroregenerative attempts, since VEGF naturally enhances neuron resistance to injury and regulates neural progenitor proliferation, migration, differentiation and oligodendrocyte precursor cell (OPC) survival and migration to demyelinated lesions. Angiogenesis, neurogenesis and oligodendroglia maturation are closely intertwined in the neurovascular niches of the subventricular zone, one of the preferential locations of inflammatory lesions in MS, and in all the other temporary vascular niches where the mutual fostering of angiogenesis and OPC maturation occurs. Angiogenesis, induced either by CNS inflammation or by hypoxic stimuli related to neurovascular uncoupling, appears to be ineffective in chronic MS due to a counterbalancing effect of vasoconstrictive mechanisms determined by the reduced axonal activity, astrocyte dysfunction, microglia secretion of free radical species and mitochondrial abnormalities. Thus, angiogenesis, that supplies several trophic factors, should be promoted in therapeutic neuroregeneration efforts to combat the progressive, degenerative phase of MS.

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Effects of atorvastatin in the regulation of circulating EPCs and angiogenesis in traumatic brain injury in rats

Cited by 59 publications

References 39 publications

Cerebral Vascular Injury in Traumatic Brain Injury

Cerebral Vascular Injury in Traumatic Brain Injury

Strategies and Techniques to Enhance theIn SituEndothelialization of Small-Diameter Biodegradable Polymeric Vascular Grafts

Angiogenesis in multiple sclerosis and experimental autoimmune encephalomyelitis

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