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Special Issue "Neuroregeneration and Brain Repair after Stroke"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (28 February 2021).

Special Issue Editor

Assoc. Prof. Yuji Ueno
E-Mail Website
Guest Editor
Department of Neurology, Juntendo University Faculty of Medicine, Tokyo 113-8421, Japan

Special Issue Information

Dear Colleagues,

Stroke is the second leading cause of death and a major cause of disability worldwide. Although acute stroke therapies such as recombinant human tissue-type plasminogen activator and endovascular thrombectomy effectively reduce mortality and alleviate neurological deficits, poor functional outcomes in stroke survivors are still present. In the chronic stage of stroke, only rehabilitation is established as a conventional strategy for functional recovery. Thus, therapies to improve functional recovery are urgently needed.

During recovery of stroke, many molecular cascades that produce inflammatory processes, spontaneous brain repair, and neuro-regeneration. Circulating endothelial progenitor cells as well as cerebral endothelial cells in survived blood vessels are involved in the mechanisms of angiogenesis. Production of neural stem and progenitor cells is promoted, and these cells are migrated to stroke lesions. Additionally, axonal outgrowth and oligodendrogenesis are facilitated in the peri-infarct gray and white matter, and regenerated and myelinated fibers contribute to repairing injured brains. On the other hand, astrocytic glial scar formation suppresses axonal regeneration with the production of inhibitory molecules.

For this Special Issue, we are seeking novel molecular mechanisms that facilitate neurogenesis and brain repair after stroke in various experimental systems. I look forward to your contributions.

Assoc. Prof. Yuji Ueno
Guest Editor

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Keywords

  • stroke
  • neurogenesis
  • axonal outgrowth
  • oligodendrogenesis
  • glial scar
  • astrocyte
  • regenerative medicine
  • restorative therapy
  • recovery
  • stem cells

Published Papers (14 papers)

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Research

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Article
C-Type Natriuretic Peptide Ameliorates Vascular Injury and Improves Neurological Outcomes in Neonatal Hypoxic-Ischemic Brain Injury in Mice
Int. J. Mol. Sci. 2021, 22(16), 8966; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22168966 - 20 Aug 2021
Viewed by 367
Abstract
C-type natriuretic peptide (CNP) is an important vascular regulator that is present in the brain. Our previous study demonstrated the innate neuroprotectant role of CNP in the neonatal brain after hypoxic-ischemic (HI) insults. In this study, we further explored the role of CNP [...] Read more.
C-type natriuretic peptide (CNP) is an important vascular regulator that is present in the brain. Our previous study demonstrated the innate neuroprotectant role of CNP in the neonatal brain after hypoxic-ischemic (HI) insults. In this study, we further explored the role of CNP in cerebrovascular pathology using both in vivo and in vitro models. In a neonatal mouse HI brain injury model, we found that intracerebroventricular administration of recombinant CNP dose-dependently reduces brain infarct size. CNP significantly decreases brain edema and immunoglobulin G (IgG) extravasation into the brain tissue, suggesting a vasculoprotective effect of CNP. Moreover, in primary brain microvascular endothelial cells (BMECs), CNP dose-dependently protects BMEC survival and monolayer integrity against oxygen-glucose deprivation (OGD). The vasculoprotective effect of CNP is mediated by its innate receptors NPR2 and NPR3, in that inhibition of either NPR2 or NPR3 counteracts the protective effect of CNP on IgG leakage after HI insult and BMEC survival under OGD. Of importance, CNP significantly ameliorates brain atrophy and improves neurological deficits after HI insults. Altogether, the present study indicates that recombinant CNP exerts vascular protection in neonatal HI brain injury via its innate receptors, suggesting a potential therapeutic target for the treatment of neonatal HI brain injury. Full article
(This article belongs to the Special Issue Neuroregeneration and Brain Repair after Stroke)
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Article
BDNF rs6265 Polymorphism and Its Methylation in Patients with Stroke Undergoing Rehabilitation
Int. J. Mol. Sci. 2020, 21(22), 8438; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21228438 - 10 Nov 2020
Cited by 2 | Viewed by 638
Abstract
Brain-Derived Neurotrophic Factor (BDNF) and its rs6265 single nucleotide polymorphism (SNP) play an important role in post-stroke recovery. We investigated the correlation between BDNF rs6265 SNP and recovery outcome, measured by the modified Barthel index, in 49 patients with stroke hospitalized in our [...] Read more.
Brain-Derived Neurotrophic Factor (BDNF) and its rs6265 single nucleotide polymorphism (SNP) play an important role in post-stroke recovery. We investigated the correlation between BDNF rs6265 SNP and recovery outcome, measured by the modified Barthel index, in 49 patients with stroke hospitalized in our rehabilitation center at baseline (T0) and after 30 sessions of rehabilitation treatment (T1); moreover, we analyzed the methylation level of the CpG site created or abolished into BDNF rs6265 SNP. In total, 11 patients (22.4%) were heterozygous GA, and 32 (65.3%) and 6 (12.2%) patients were homozygous GG and AA, respectively. The univariate analysis showed a significant relationship between the BDNF rs6265 SNP and the modified Barthel index cut-off (χ2(1, N = 48) = 3.86, p = 0.049), considering patients divided for carrying (A+) or not carrying (A−) the A allele. A higher percentage of A− patients obtained a favorable outcome, as showed by the logistic regression model corrected by age and time since the stroke onset, compared with the A+ patients (OR: 5.59). At baseline (T0), the percentage of BDNF methylation was significantly different between GG (44.6 ± 1.1%), GA (39.5 ± 2.8%) and AA (28.5 ± 1.7%) alleles (p < 0.001). After rehabilitation (T1), only patients A− showed a significant increase in methylation percentages (mean change = 1.3, CI: 0.4–2.2, p = 0.007). This preliminary study deserves more investigation to confirm if BDNF rs6265 SNP and its methylation could be used as a biological marker of recovery in patients with stroke undergoing rehabilitation treatment. Full article
(This article belongs to the Special Issue Neuroregeneration and Brain Repair after Stroke)
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Article
The Fate of Transplanted Olfactory Progenitors Is Conditioned by the Cell Phenotypes of the Receiver Brain Tissue in Cocultures
Int. J. Mol. Sci. 2020, 21(19), 7249; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21197249 - 30 Sep 2020
Viewed by 762
Abstract
Among the numerous candidates for cell therapy of the central nervous system (CNS), olfactory progenitors (OPs) represent an interesting alternative because they are free of ethical concerns, are easy to collect, and allow autologous transplantation. In the present study, we focused on the [...] Read more.
Among the numerous candidates for cell therapy of the central nervous system (CNS), olfactory progenitors (OPs) represent an interesting alternative because they are free of ethical concerns, are easy to collect, and allow autologous transplantation. In the present study, we focused on the optimization of neuron production and maturation. It is known that plated OPs respond to various trophic factors, and we also showed that the use of Nerve Growth Factor (NGF) allowed switching from a 60/40 neuron/glia ratio to an 80/20 one. Nevertheless, in order to focus on the integration of OPs in mature neural circuits, we cocultured OPs in primary cultures obtained from the cortex and hippocampus of newborn mice. When dissociated OPs were plated, they differentiated into both glial and neuronal phenotypes, but we obtained a 1.5-fold higher viability in cortex/OP cocultures than in hippocampus/OP ones. The fate of OPs in cocultures was characterized with different markers such as BrdU, Map-2, and Synapsin, indicating a healthy integration. These results suggest that the integration of transplanted OPs might by affected by trophic factors and the environmental conditions/cell phenotypes of the host tissue. Thus, a model of coculture could provide useful information on key cell events for the use of progenitors in cell therapy. Full article
(This article belongs to the Special Issue Neuroregeneration and Brain Repair after Stroke)
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Article
The Role of Losartan as a Potential Neuroregenerative Pharmacological Agent after Aneurysmal Subarachnoid Haemorrhage
Int. J. Mol. Sci. 2020, 21(18), 6496; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21186496 - 05 Sep 2020
Cited by 1 | Viewed by 668
Abstract
Background: Cerebral vasospasm (CVS) remains a major cause of delayed cerebral ischaemia following aneurysmal subarachnoid haemorrhage (SAH), making it a life-threatening type of stroke with high morbidity and mortality. Endothelin-1 is known as key player mediating a strong vasocontractile effect. Interestingly, losartan restores [...] Read more.
Background: Cerebral vasospasm (CVS) remains a major cause of delayed cerebral ischaemia following aneurysmal subarachnoid haemorrhage (SAH), making it a life-threatening type of stroke with high morbidity and mortality. Endothelin-1 is known as key player mediating a strong vasocontractile effect. Interestingly, losartan restores the impaired vasorelaxative ET(B1) receptor function in a non-competitive direct fashion. With this study, we aimed to investigate a potential losartan-dependent vasodilatory effect vice versa by inhibiting NO release through L-NAME, thus pushing forward concepts to alleviate vasospasm and possibly prevent ischaemia and neurodegeneration. Methods: Cerebral vasospasm was induced by the use of an established double-injection rat model. Sprague-Dawley rats were culled on Day 3 after the ictus, and the vasospastic basilar artery was harvested for isometric investigations of the vessel tone. Ring segments were preincubated with and without L-NAME and/or losartan. Results: Preincubation with L-NAME induced dose-dependent vasoconstriction via endothelin-1 in the non-SAH cohort, which was dose-dependently reduced by losartan. After SAH and dose-dependent endothelin-1 administration, maximal contraction was achieved in the control group without losartan. Furthermore, this maximal contraction was significantly decreased in the losartan group and was reversed by L-NAME. Conclusions: After SAH, losartan was shown to positively influence the ET(B1) receptor pathway in a non-competitive direct agonistic and indirect fashion. Losartan alleviated the maximum contraction triggered by endothelin-1. This effect was resolved due to NO inhibition by L-NAME. Considering this spasmolytic effect of losartan besides its already well-known effects (attenuating cerebral inflammation, restoring cerebral autoregulation and reducing epileptogenic activity) and alleviating early brain injury, losartan seems to have potential as a promising pharmacological agent after SAH. Full article
(This article belongs to the Special Issue Neuroregeneration and Brain Repair after Stroke)
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Article
Neurodegeneration, Myelin Loss and Glial Response in the Three-Vessel Global Ischemia Model in Rat
Int. J. Mol. Sci. 2020, 21(17), 6246; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21176246 - 28 Aug 2020
Cited by 2 | Viewed by 887
Abstract
(1) Background: Although myelin disruption is an integral part of ischemic brain injury, it is rarely the subject of research, particularly in animal models. This study assessed for the first time, myelin and oligodendrocyte loss in a three-vessel model of global cerebral ischemia [...] Read more.
(1) Background: Although myelin disruption is an integral part of ischemic brain injury, it is rarely the subject of research, particularly in animal models. This study assessed for the first time, myelin and oligodendrocyte loss in a three-vessel model of global cerebral ischemia (GCI), which causes hippocampal damage. In addition, we investigated the relationships between demyelination and changes in microglia and astrocytes, as well as oligodendrogenesis in the hippocampus; (2) Methods: Adult male Wistar rats (n = 15) underwent complete interruption of cerebral blood flow for 7 min by ligation of the major arteries supplying the brain or sham-operation. At 10 and 30 days after the surgery, brain slices were stained for neurodegeneration with Fluoro-Jade C and immunohistochemically to assess myelin content (MBP+ percentage of total area), oligodendrocyte (CNP+ cells) and neuronal (NeuN+ cells) loss, neuroinflammation (Iba1+ cells), astrogliosis (GFAP+ cells) and oligodendrogenesis (NG2+ cells); (3) Results: 10 days after GCI significant myelin and oligodendrocyte loss was found only in the stratum oriens and stratum pyramidale. By the 30th day, demyelination in these hippocampal layers intensified and affected the substratum radiatum. In addition to myelin damage, activation and an increase in the number of microglia and astrocytes in the corresponding layers, a loss of the CA1 pyramidal neurons, and neurodegeneration in the neocortex and thalamus was observed. At a 10-day time point, we observed rod-shaped microglia in the substratum radiatum. Parallel with ongoing myelin loss on the 30th day after ischemia, we found significant oligodendrogenesis in demyelinated hippocampal layers; (4) Conclusions: Our study showed that GCI-simulating cardiac arrest in humans—causes not only the loss of pyramidal neurons in the CA1 field, but also the myelin loss of adjacent layers of the hippocampus. Full article
(This article belongs to the Special Issue Neuroregeneration and Brain Repair after Stroke)
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Article
Growth Hormone Treatment Promotes Remote Hippocampal Plasticity after Experimental Cortical Stroke
Int. J. Mol. Sci. 2020, 21(12), 4563; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21124563 - 26 Jun 2020
Cited by 6 | Viewed by 1637
Abstract
Cognitive impairment is common after stroke, and disturbances in hippocampal function are often involved, even in remote non-hippocampal injuries. In terms of hippocampal function, growth hormone (GH) is known to affects plasticity and cognition. We aimed to investigate whether GH treatment after an [...] Read more.
Cognitive impairment is common after stroke, and disturbances in hippocampal function are often involved, even in remote non-hippocampal injuries. In terms of hippocampal function, growth hormone (GH) is known to affects plasticity and cognition. We aimed to investigate whether GH treatment after an experimental cortical stroke could enhance remote hippocampal plasticity and the hippocampal-dependent visual discrimination task. C57BL6 male mice were subjected to cortical photothrombotic stroke. Stroke mice were then treated with either saline or GH at 48 h after occlusion for 28 days. We assessed learning and memory using mouse touchscreen platform for the visual discrimination task. We also evaluated markers of neural progenitor cells, synaptic plasticity and cerebrovascular remodelling in the hippocampal formation. GH treatment significantly improved the performance on visual discrimination task after stroke. We observed a concomitant increased number of bromodeoxyuridine-positive cells in the dentate gyrus of the hippocampus. We also detected increased protein levels and density of doublecortin, a neuronal precursor cells marker, as well as glutamate receptor 1 (GLuR1), a synaptic marker. These findings provide further neurobiological evidence for how GH treatment could be used to promote hippocampal plasticity in a remote region from the initial cortical injury, and thus enhance cognitive recovery after stroke. Full article
(This article belongs to the Special Issue Neuroregeneration and Brain Repair after Stroke)
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Review

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Review
Astrocyte Activation in Neurovascular Damage and Repair Following Ischaemic Stroke
Int. J. Mol. Sci. 2021, 22(8), 4280; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22084280 - 20 Apr 2021
Cited by 2 | Viewed by 898
Abstract
Transient or permanent loss of tissue perfusion due to ischaemic stroke can lead to damage to the neurovasculature, and disrupt brain homeostasis, causing long-term motor and cognitive deficits. Despite promising pre-clinical studies, clinically approved neuroprotective therapies are lacking. Most studies have focused on [...] Read more.
Transient or permanent loss of tissue perfusion due to ischaemic stroke can lead to damage to the neurovasculature, and disrupt brain homeostasis, causing long-term motor and cognitive deficits. Despite promising pre-clinical studies, clinically approved neuroprotective therapies are lacking. Most studies have focused on neurons while ignoring the important roles of other cells of the neurovascular unit, such as astrocytes and pericytes. Astrocytes are important for the development and maintenance of the blood–brain barrier, brain homeostasis, structural support, control of cerebral blood flow and secretion of neuroprotective factors. Emerging data suggest that astrocyte activation exerts both beneficial and detrimental effects following ischaemic stroke. Activated astrocytes provide neuroprotection and contribute to neurorestoration, but also secrete inflammatory modulators, leading to aggravation of the ischaemic lesion. Astrocytes are more resistant than other cell types to stroke pathology, and exert a regulative effect in response to ischaemia. These roles of astrocytes following ischaemic stroke remain incompletely understood, though they represent an appealing target for neurovascular protection following stroke. In this review, we summarise the astrocytic contributions to neurovascular damage and repair following ischaemic stroke, and explore mechanisms of neuroprotection that promote revascularisation and neurorestoration, which may be targeted for developing novel therapies for ischaemic stroke. Full article
(This article belongs to the Special Issue Neuroregeneration and Brain Repair after Stroke)
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Review
Is High-Intensity Interval Training Suitable to Promote Neuroplasticity and Cognitive Functions after Stroke?
Int. J. Mol. Sci. 2021, 22(6), 3003; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22063003 - 16 Mar 2021
Viewed by 1407
Abstract
Stroke-induced cognitive impairments affect the long-term quality of life. High-intensity interval training (HIIT) is now considered a promising strategy to enhance cognitive functions. This review is designed to examine the role of HIIT in promoting neuroplasticity processes and/or cognitive functions after stroke. The [...] Read more.
Stroke-induced cognitive impairments affect the long-term quality of life. High-intensity interval training (HIIT) is now considered a promising strategy to enhance cognitive functions. This review is designed to examine the role of HIIT in promoting neuroplasticity processes and/or cognitive functions after stroke. The various methodological limitations related to the clinical relevance of studies on the exercise recommendations in individuals with stroke are first discussed. Then, the relevance of HIIT in improving neurotrophic factors expression, neurogenesis and synaptic plasticity is debated in both stroke and healthy individuals (humans and rodents). Moreover, HIIT may have a preventive role on stroke severity, as found in rodents. The potential role of HIIT in stroke rehabilitation is reinforced by findings showing its powerful neurogenic effect that might potentiate cognitive benefits induced by cognitive tasks. In addition, the clinical role of neuroplasticity observed in each hemisphere needs to be clarified by coupling more frequently to cellular/molecular measurements and behavioral testing. Full article
(This article belongs to the Special Issue Neuroregeneration and Brain Repair after Stroke)
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Review
Neurotrophins Time Point Intervention after Traumatic Brain Injury: From Zebrafish to Human
Int. J. Mol. Sci. 2021, 22(4), 1585; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22041585 - 04 Feb 2021
Cited by 1 | Viewed by 900
Abstract
Traumatic brain injury (TBI) remains the leading cause of long-term disability, which annually involves millions of individuals. Several studies on mammals reported that neurotrophins could play a significant role in both protection and recovery of function following neurodegenerative diseases such as stroke and [...] Read more.
Traumatic brain injury (TBI) remains the leading cause of long-term disability, which annually involves millions of individuals. Several studies on mammals reported that neurotrophins could play a significant role in both protection and recovery of function following neurodegenerative diseases such as stroke and TBI. This protective role of neurotrophins after an event of TBI has also been reported in the zebrafish model. Nevertheless, reparative mechanisms in mammalian brain are limited, and newly formed neurons do not survive for a long time. In contrast, the brain of adult fish has high regenerative properties after brain injury. The evident differences in regenerative properties between mammalian and fish brain have been ascribed to remarkable different adult neurogenesis processes. However, it is not clear if the specific role and time point contribution of each neurotrophin and receptor after TBI is conserved during vertebrate evolution. Therefore, in this review, I reported the specific role and time point of intervention for each neurotrophic factor and receptor after an event of TBI in zebrafish and mammals. Full article
(This article belongs to the Special Issue Neuroregeneration and Brain Repair after Stroke)
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Review
Pleiotropic Effects of Exosomes as a Therapy for Stroke Recovery
Int. J. Mol. Sci. 2020, 21(18), 6894; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21186894 - 20 Sep 2020
Cited by 5 | Viewed by 1142
Abstract
Stroke is the leading cause of disability, and stroke survivors suffer from long-term sequelae even after receiving recombinant tissue plasminogen activator therapy and endovascular intracranial thrombectomy. Increasing evidence suggests that exosomes, nano-sized extracellular membrane vesicles, enhance neurogenesis, angiogenesis, and axonal outgrowth, all the [...] Read more.
Stroke is the leading cause of disability, and stroke survivors suffer from long-term sequelae even after receiving recombinant tissue plasminogen activator therapy and endovascular intracranial thrombectomy. Increasing evidence suggests that exosomes, nano-sized extracellular membrane vesicles, enhance neurogenesis, angiogenesis, and axonal outgrowth, all the while suppressing inflammatory reactions, thereby enhancing functional recovery after stroke. A systematic literature review to study the association of stroke recovery with exosome therapy was carried out, analyzing species, stroke model, source of exosomes, behavioral analyses, and outcome data, as well as molecular mechanisms. Thirteen studies were included in the present systematic review. In the majority of studies, exosomes derived from mesenchymal stromal cells or stem cells were administered intravenously within 24 h after transient middle cerebral artery occlusion, showing a significant improvement of neurological severity and motor functions. Specific microRNAs and molecules were identified by mechanistic investigations, and their amplification was shown to further enhance therapeutic effects, including neurogenesis, angiogenesis, axonal outgrowth, and synaptogenesis. Overall, this review addresses the current advances in exosome therapy for stroke recovery in preclinical studies, which can hopefully be preparatory steps for the future development of clinical trials involving stroke survivors to improve functional outcomes. Full article
(This article belongs to the Special Issue Neuroregeneration and Brain Repair after Stroke)
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Review
Recent Advances in Cell-Based Therapies for Ischemic Stroke
Int. J. Mol. Sci. 2020, 21(18), 6718; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21186718 - 14 Sep 2020
Cited by 10 | Viewed by 1564
Abstract
Stroke is the most prevalent cardiovascular disease worldwide, and is still one of the leading causes of death and disability. Stem cell-based therapy is actively being investigated as a new potential treatment for certain neurological disorders, including stroke. Various types of cells, including [...] Read more.
Stroke is the most prevalent cardiovascular disease worldwide, and is still one of the leading causes of death and disability. Stem cell-based therapy is actively being investigated as a new potential treatment for certain neurological disorders, including stroke. Various types of cells, including bone marrow mononuclear cells, bone marrow mesenchymal stem cells, dental pulp stem cells, neural stem cells, inducible pluripotent stem cells, and genetically modified stem cells have been found to improve neurological outcomes in animal models of stroke, and there are some ongoing clinical trials assessing their efficacy in humans. In this review, we aim to summarize the recent advances in cell-based therapies to treat stroke. Full article
(This article belongs to the Special Issue Neuroregeneration and Brain Repair after Stroke)
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Review
Epigenetic Mechanisms Underlying Adult Post Stroke Neurogenesis
Int. J. Mol. Sci. 2020, 21(17), 6179; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21176179 - 27 Aug 2020
Cited by 2 | Viewed by 1049
Abstract
Stroke remains the leading cause of adult disability. Post-stroke neurogenesis contributes to functional recovery. As an intrinsic neurorestorative process, it is important to elucidate the molecular mechanism underlying stroke-induced neurogenesis and to develop therapies designed specifically to augment neurogenesis. Epigenetic mechanisms include DNA [...] Read more.
Stroke remains the leading cause of adult disability. Post-stroke neurogenesis contributes to functional recovery. As an intrinsic neurorestorative process, it is important to elucidate the molecular mechanism underlying stroke-induced neurogenesis and to develop therapies designed specifically to augment neurogenesis. Epigenetic mechanisms include DNA methylation, histone modification and its mediation by microRNAs and long-non-coding RNAs. In this review, we highlight how epigenetic factors including DNA methylation, histone modification, microRNAs and long-non-coding RNAs mediate stroke-induced neurogenesis including neural stem cell self-renewal and cell fate determination. We also summarize therapies targeting these mechanisms in the treatment of stroke. Full article
(This article belongs to the Special Issue Neuroregeneration and Brain Repair after Stroke)
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Review
Current Synthesis and Systematic Review of Main Effects of Calf Blood Deproteinized Medicine (Actovegin®) in Ischemic Stroke
Int. J. Mol. Sci. 2020, 21(9), 3181; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21093181 - 30 Apr 2020
Cited by 5 | Viewed by 953
Abstract
Background: Stroke is one of the largest problems and clinical-social challenges within neurology and, in general, pathology. Here, we briefly reviewed the main pathophysiological mechanisms of ischemic stroke, which represent targets for medical interventions, including for a calf blood deproteinized hemodialysate/ultrafiltrate. Methods: We [...] Read more.
Background: Stroke is one of the largest problems and clinical-social challenges within neurology and, in general, pathology. Here, we briefly reviewed the main pathophysiological mechanisms of ischemic stroke, which represent targets for medical interventions, including for a calf blood deproteinized hemodialysate/ultrafiltrate. Methods: We conducted a systematic review of current related literature concerning the effects of Actovegin®, of mainly the pleiotropic type, applied to the injury pathways of ischemic stroke. Results: The bibliographic resources regarding the use of Actovegin® in ischemic stroke are scarce. The main Actovegin® actions refer to the ischemic stroke lesion items’ ensemble, targeting tissue oxidation, energy metabolism, and glucose availability through their augmentation, combating ischemic processes and oxidative stress, and decreasing inflammation (including with modulatory connotations, by the nuclear factor-κB pathway) and apoptosis-like processes, counteracting them by mitigating the caspase-3 activation induced by amyloid β-peptides. Conclusion: Since no available therapeutic agents are capable of curing the central nervous system’s lesions, any contribution, such as that of Actovegin® (with consideration of a positive balance between benefits and risks), is worthy of further study and periodic reappraisal, including investigation into further connected aspects. Full article
(This article belongs to the Special Issue Neuroregeneration and Brain Repair after Stroke)
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Review
Brain–Heart Axis and Biomarkers of Cardiac Damage and Dysfunction after Stroke: A Systematic Review and Meta-Analysis
Int. J. Mol. Sci. 2020, 21(7), 2347; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21072347 - 28 Mar 2020
Cited by 3 | Viewed by 1382
Abstract
Background: Cardiac complications after a stroke are the second leading cause of death worldwide, affecting the treatment and outcomes of stroke patients. Cardiac biomarkers such as cardiac troponin (cTn), brain natriuretic peptide (BNP), and N-terminal pro-brain natriuretic peptide (NT-proBNP) have been frequently reported [...] Read more.
Background: Cardiac complications after a stroke are the second leading cause of death worldwide, affecting the treatment and outcomes of stroke patients. Cardiac biomarkers such as cardiac troponin (cTn), brain natriuretic peptide (BNP), and N-terminal pro-brain natriuretic peptide (NT-proBNP) have been frequently reported in patients undergoing a stroke. The aim of the present study is to meta-analyze the relationship between changes in such cardiac biomarkers and stroke and to present a systematic review of the previous literature, so as to explore the brain–heart axis. Methods: We searched four online databases pertinent to the literature, including PubMed, Embase, the Cochrane Library, and the Web of Science. Then, we performed a meta-analysis to investigate changes in cTn, BNP, and NT-proBNP associated with different types of stroke. Results and Conclusions: A significant increase in cTnI concentration was found in patients exhibiting a brain hemorrhage. BNP increased in cases of brain infarction, while the NT-proBNP concentration was significantly elevated in patients suffering an acute ischemic stroke and brain hemorrhage, indicating cardiac damage and dysfunction after a stroke. Our analysis suggests that several potential mechanisms may be involved in the brain–heart axis. Finally, clinicians should pay careful attention to monitoring cardiac function in the treatment of cerebrovascular diseases in order to provide a timely and more accurate treatment. Full article
(This article belongs to the Special Issue Neuroregeneration and Brain Repair after Stroke)
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