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Neuron Cell Death

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

Deadline for manuscript submissions: closed (15 September 2018) | Viewed by 103981

Special Issue Editors

Department of Veterinary Sciences, University of Turin, Turin, Italy
Interests: pain; somatosensory pathways; spinal cord; neuron death; cerebellum; development; neuronal circuits
Department of Veterinary Clinical Sciences, Universita degli Studi di Torino, Torino, Italy
Interests: apoptosis; programmed cell death; caspases; death receptors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The discovery of neuronal cell death dates back to the 19th century. Nowadays, the notion that cell death is a phenomenon occurring during the entire life course of the nervous system, from neurogenesis to adulthood and old age, is fully established. Moreover, it is widely accepted that death of neurons occurs in certain pathologies of the brain, including neurodegenerative diseases. The dichotomy between apoptosis, as the prototype of programmed cell death (PCD), and necrosis, as the prototype of death caused by an external insult, must be carefully reconsidered, as different types of PCD including apoptosis, autophagy, pyroptosis, and oncosis have all been demonstrated in neurons. These modes of PCD may be triggered by different stimuli, but share some intracellular pathways such that different types of cell death may affect the same population of neurons according to several intrinsic and extrinsic factors, so that a mixed morphology is often observed also depending on degrees of differentiation, activity and injury.

This Special Issue focuses on the recent progress in understanding the cellular and molecular biology of the death of central neurons, as well as the underlying mechanisms of PCD in the normal and pathological brain. Molecular alterations of these mechanisms represent promising diagnostic and prognostic molecular markers and therapeutic targets for neurodegenerative diseases and age-related cognitive impairment. The discovery of specific biomarkers, as well as the specific changes in gene expression patterns and alterations of the normal protein profile of the nerve cell in cell culture and animal will also be considered in this Special Issue.

Prof. Dr. Adalberto Merighi
Prof. Dr. Laura Lossi
Guest Editors

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Keywords

  • Neurons
  • Cell death
  • Apoptosis
  • Oncosis
  • Pyroptosis
  • Autophagy
  • Neurogenesis
  • Aging
  • Neurodegeneration
  • Programmed cell death
  • Necrosis

Published Papers (12 papers)

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Research

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16 pages, 3705 KiB  
Article
Chaperone-E3 Ligase Complex HSP70-CHIP Mediates Ubiquitination of Ribosomal Protein S3
by Inwoo Hwang, Sung-Woo Cho and Jee-Yin Ahn
Int. J. Mol. Sci. 2018, 19(9), 2723; https://doi.org/10.3390/ijms19092723 - 12 Sep 2018
Cited by 8 | Viewed by 6081
Abstract
In addition to its role in ribosome biogenesis, ribosomal protein S3 (RPS3), a component of the 40S ribosomal subunit, has been suggested to possess several extraribosomal functions, including an apoptotic function. In this study, we demonstrated that in the mouse brain, the protein [...] Read more.
In addition to its role in ribosome biogenesis, ribosomal protein S3 (RPS3), a component of the 40S ribosomal subunit, has been suggested to possess several extraribosomal functions, including an apoptotic function. In this study, we demonstrated that in the mouse brain, the protein levels of RPS3 were altered by the degree of nutritional starvation and correlated with neuronal apoptosis. After endurable short-term starvation, the apoptotic function of RPS3 was suppressed by Akt activation and Akt-mediated T70 phosphorylation, whereas after prolonged starvation, the protein levels of RPS3 notably increased, and abundant neuronal death occurred. These events coincided with ubiquitination and subsequent degradation of RPS3, controlled by HSP70 and the cochaperone E3 ligase: carboxy terminus of heat shock protein 70-interacting protein (CHIP). Thus, our study points to an extraribosomal role of RPS3 in balancing neuronal survival or death depending on the degree of starvation through CHIP-mediated polyubiquitination and degradation. Full article
(This article belongs to the Special Issue Neuron Cell Death)
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25 pages, 7030 KiB  
Article
AAV-Syn-BDNF-EGFP Virus Construct Exerts Neuroprotective Action on the Hippocampal Neural Network during Hypoxia In Vitro
by Elena V. Mitroshina, Tatiana A. Mishchenko, Alexandra V. Usenko, Ekaterina A. Epifanova, Roman S. Yarkov, Maria S. Gavrish, Alexey A. Babaev and Maria V. Vedunova
Int. J. Mol. Sci. 2018, 19(8), 2295; https://doi.org/10.3390/ijms19082295 - 05 Aug 2018
Cited by 18 | Viewed by 4927
Abstract
Brain-derived neurotrophic factor (BDNF) is one of the key signaling molecules that supports the viability of neural cells in various brain pathologies, and can be considered a potential therapeutic agent. However, several methodological difficulties, such as overcoming the blood–brain barrier and the short [...] Read more.
Brain-derived neurotrophic factor (BDNF) is one of the key signaling molecules that supports the viability of neural cells in various brain pathologies, and can be considered a potential therapeutic agent. However, several methodological difficulties, such as overcoming the blood–brain barrier and the short half-life period, challenge the potential use of BDNF in clinical practice. Gene therapy could overcome these limitations. Investigating the influence of viral vectors on the neural network level is of particular interest because viral overexpression affects different aspects of cell metabolism and interactions between neurons. The present work aimed to investigate the influence of the adeno-associated virus (AAV)-Syn-BDNF-EGFP virus construct on neural network activity parameters in an acute hypobaric hypoxia model in vitro. Materials and methods. An adeno-associated virus vector carrying the BDNF gene was constructed using the following plasmids: AAV-Syn-EGFP, pDP5, DJvector, and pHelper. The developed virus vector was then tested on primary hippocampal cultures obtained from C57BL/6 mouse embryos (E18). Acute hypobaric hypoxia was induced on day 21 in vitro. Spontaneous bioelectrical and calcium activity of neural networks in primary cultures and viability tests were analysed during normoxia and during the posthypoxic period. Results. BDNF overexpression by AAV-Syn-BDNF-EGFP does not affect cell viability or the main parameters of spontaneous bioelectrical activity in normoxia. Application of the developed virus construct partially eliminates the negative hypoxic consequences by preserving cell viability and maintaining spontaneous bioelectrical activity in the cultures. Moreover, the internal functional structure, including the activation pattern of network bursts, the number of hubs, and the number of connections within network elements, is also partially preserved. BDNF overexpression prevents a decrease in the number of cells exhibiting calcium activity and maintains the frequency of calcium oscillations. Conclusion. This study revealed the pronounced antihypoxic and neuroprotective effects of AAV-Syn-BDNF-EGFP virus transduction in an acute normobaric hypoxia model. Full article
(This article belongs to the Special Issue Neuron Cell Death)
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14 pages, 3662 KiB  
Article
Pharmacological Basis for the Use of Evodiamine in Alzheimer’s Disease: Antioxidation and Antiapoptosis
by Yongfeng Zhang, Jiaqi Wang, Chunyue Wang, Zhiping Li, Xin Liu, Jun Zhang, Jiahui Lu and Di Wang
Int. J. Mol. Sci. 2018, 19(5), 1527; https://doi.org/10.3390/ijms19051527 - 21 May 2018
Cited by 36 | Viewed by 5290
Abstract
Evodiamine (Evo), a major alkaloid compound isolated from the dry unripened fruit of Evodia fructus, has a wide range of pharmacological activities. The present study sought to explore the neuroprotective effects of Evo in l-glutamate (l-Glu)-induced apoptosis of HT22 cells, [...] Read more.
Evodiamine (Evo), a major alkaloid compound isolated from the dry unripened fruit of Evodia fructus, has a wide range of pharmacological activities. The present study sought to explore the neuroprotective effects of Evo in l-glutamate (l-Glu)-induced apoptosis of HT22 cells, and in a d-galactose and aluminum trichloride-developed Alzheimer’s disease (AD) mouse model. Evo significantly enhanced cell viability, inhibited the accumulation of reactive oxygen species, ameliorated mitochondrial function, increased the B-cell lymphoma-2 protein content, and inhibited the high expression levels of Bax, Bad, and cleaved-caspase-3 and -8 in l-Glu-induced HT22 cells. Evo also enhanced the phosphorylation activities of protein kinase B and the mammalian target of rapamycin in the l-Glu-induced HT22 cells. In the AD mouse model, Evo reduced the aimless and chaotic movements, reduced the time spent in the central area in the open field test, and decreased the escape latency time in the Morris water maze test. Evo reduced the deposition of amyloid beta 42 (Aβ42) in the brain, and increased the serum level of Aβ42, but showed no significant effects on Aβ40. In addition, six weeks of Evo administration significantly suppressed oxidative stress by modulating the related enzyme levels. In the central cholinergic system of AD mice, Evo significantly increased the serum levels of acetylcholine and choline acetyltransferase and decreased the level of acetylcholinesterase in the serum, hypothalamus, and brain. Our results provide experimental evidence that Evo can serve as a neuroprotective candidate for the prevention and/or treatment of neurodegenerative diseases. Full article
(This article belongs to the Special Issue Neuron Cell Death)
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12 pages, 15945 KiB  
Article
Neuronal Dysfunction Associated with Cholesterol Deregulation
by Annalisa Marcuzzi, Claudia Loganes, Erica Valencic, Elisa Piscianz, Lorenzo Monasta, Sabrine Bilel, Roberta Bortul, Claudio Celeghini, Marina Zweyer and Alberto Tommasini
Int. J. Mol. Sci. 2018, 19(5), 1523; https://doi.org/10.3390/ijms19051523 - 19 May 2018
Cited by 10 | Viewed by 4859
Abstract
Cholesterol metabolism is crucial for cells and, in particular, its biosynthesis in the central nervous system occurs in situ, and its deregulation involves morphological changes that cause functional variations and trigger programmed cell death. The pathogenesis of rare diseases, such as Mevalonate Kinase [...] Read more.
Cholesterol metabolism is crucial for cells and, in particular, its biosynthesis in the central nervous system occurs in situ, and its deregulation involves morphological changes that cause functional variations and trigger programmed cell death. The pathogenesis of rare diseases, such as Mevalonate Kinase Deficiency or Smith–Lemli–Opitz Syndrome, arises due to enzymatic defects in the cholesterol metabolic pathways, resulting in a shortage of downstream products. The most severe clinical manifestations of these diseases appear as neurological defects. Expanding the knowledge of this biological mechanism will be useful for identifying potential targets and preventing neuronal damage. Several studies have demonstrated that deregulation of the cholesterol pathway induces mitochondrial dysfunction as the result of respiratory chain damage. We set out to determine whether mitochondrial damage may be prevented by using protective mitochondria-targeted compounds, such as MitoQ, in a neuronal cell line treated with a statin to induce a biochemical block of the cholesterol pathway. Evidence from the literature suggests that mitochondria play a crucial role in the apoptotic mechanism secondary to blocking the cholesterol pathway. Our study shows that MitoQ, administered as a preventive agent, could counteract the cell damage induced by statins in the early stages, but its protective role fades over time. Full article
(This article belongs to the Special Issue Neuron Cell Death)
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12 pages, 7527 KiB  
Article
Protective Effects of Protocatechuic Acid on Seizure-Induced Neuronal Death
by Song Hee Lee, Bo Young Choi, A Ra Kho, Jeong Hyun Jeong, Dae Ki Hong, Sang Hwon Lee, Sang Yup Lee, Min Woo Lee, Hong Ki Song, Hui Chul Choi and Sang Won Suh
Int. J. Mol. Sci. 2018, 19(1), 187; https://doi.org/10.3390/ijms19010187 - 08 Jan 2018
Cited by 24 | Viewed by 4507
Abstract
Protocatechuic acid (PCA) is a type of phenolic acid found in green tea and has been shown to have potent antioxidant and anti-inflammatory properties. However, the effect of PCA on pilocarpine seizure-induced neuronal death in the hippocampus has not been evaluated. In the [...] Read more.
Protocatechuic acid (PCA) is a type of phenolic acid found in green tea and has been shown to have potent antioxidant and anti-inflammatory properties. However, the effect of PCA on pilocarpine seizure-induced neuronal death in the hippocampus has not been evaluated. In the present study, we investigated the potential therapeutic effects of PCA on seizure-induced brain injury. Epileptic seizure was induced by intraperitoneal (i.p.) injection of pilocarpine (25 mg/kg) in adult male rats, and PCA (30 mg/kg) was injected into the intraperitoneal space for three consecutive days after the seizure. Neuronal injury and oxidative stress were evaluated three days after a seizure. To confirm whether PCA increases neuronal survival and reduced oxidative injury in the hippocampus, we performed Fluoro-Jade-B (FJB) staining to detect neuronal death and 4-hydroxynonenal (4HNE) staining to detect oxidative stress after the seizure. In the present study, we found that, compared to the seizure vehicle-treated group, PCA administration reduced neuronal death and oxidative stress in the hippocampus. To verify whether a decrease of neuronal death by PCA treatment was due to reduced glutathione (GSH) concentration, we measured glutathione with N-ethylmaleimide (GS-NEM) levels in hippocampal neurons. A seizure-induced reduction in the hippocampal neuronal GSH concentration was preserved by PCA treatment. We also examined whether microglia activation was affected by the PCA treatment after a seizure, using CD11b staining. Here, we found that seizure-induced microglia activation was significantly reduced by the PCA treatment. Therefore, the present study demonstrates that PCA deserves further investigation as a therapeutic agent for reducing hippocampal neuronal death after epileptic seizures. Full article
(This article belongs to the Special Issue Neuron Cell Death)
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Review

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23 pages, 1819 KiB  
Review
Caspase-3 Mediated Cell Death in the Normal Development of the Mammalian Cerebellum
by Laura Lossi, Claudia Castagna and Adalberto Merighi
Int. J. Mol. Sci. 2018, 19(12), 3999; https://doi.org/10.3390/ijms19123999 - 12 Dec 2018
Cited by 132 | Viewed by 7580
Abstract
Caspase-3, onto which there is a convergence of the intrinsic and extrinsic apoptotic pathways, is the main executioner of apoptosis. We here review the current literature on the intervention of the protease in the execution of naturally occurring neuronal death (NOND) during cerebellar [...] Read more.
Caspase-3, onto which there is a convergence of the intrinsic and extrinsic apoptotic pathways, is the main executioner of apoptosis. We here review the current literature on the intervention of the protease in the execution of naturally occurring neuronal death (NOND) during cerebellar development. We will consider data on the most common altricial species (rat, mouse and rabbit), as well as humans. Among the different types of neurons and glia in cerebellum, there is ample evidence for an intervention of caspase-3 in the regulation of NOND of the post-mitotic cerebellar granule cells (CGCs) and Purkinje neurons, as a consequence of failure to establish proper synaptic contacts with target (secondary cell death). It seems possible that the GABAergic interneurons also undergo a similar type of secondary cell death, but the intervention of caspase-3 in this case still remains to be clarified in full. Remarkably, CGCs also undergo primary cell death at the precursor/pre-migratory stage of differentiation, in this instance without the intervention of caspase-3. Glial cells, as well, undergo a process of regulated cell death, but it seems possible that expression of caspase-3, at least in the Bergmann glia, is related to differentiation rather than death. Full article
(This article belongs to the Special Issue Neuron Cell Death)
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28 pages, 1076 KiB  
Review
Wnt/β-Catenin Signaling Pathway Governs a Full Program for Dopaminergic Neuron Survival, Neurorescue and Regeneration in the MPTP Mouse Model of Parkinson’s Disease
by Bianca Marchetti
Int. J. Mol. Sci. 2018, 19(12), 3743; https://doi.org/10.3390/ijms19123743 - 24 Nov 2018
Cited by 79 | Viewed by 12638
Abstract
Wingless-type mouse mammary tumor virus (MMTV) integration site (Wnt) signaling is one of the most critical pathways in developing and adult tissues. In the brain, Wnt signaling contributes to different neurodevelopmental aspects ranging from differentiation to axonal extension, synapse formation, neurogenesis, and neuroprotection. [...] Read more.
Wingless-type mouse mammary tumor virus (MMTV) integration site (Wnt) signaling is one of the most critical pathways in developing and adult tissues. In the brain, Wnt signaling contributes to different neurodevelopmental aspects ranging from differentiation to axonal extension, synapse formation, neurogenesis, and neuroprotection. Canonical Wnt signaling is mediated mainly by the multifunctional β-catenin protein which is a potent co-activator of transcription factors such as lymphoid enhancer factor (LEF) and T-cell factor (TCF). Accumulating evidence points to dysregulation of Wnt/β-catenin signaling in major neurodegenerative disorders. This review highlights a Wnt/β-catenin/glial connection in Parkinson’s disease (PD), the most common movement disorder characterized by the selective death of midbrain dopaminergic (mDAergic) neuronal cell bodies in the subtantia nigra pars compacta (SNpc) and gliosis. Major findings of the last decade document that Wnt/β-catenin signaling in partnership with glial cells is critically involved in each step and at every level in the regulation of nigrostriatal DAergic neuronal health, protection, and regeneration in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD, focusing on Wnt/β-catenin signaling to boost a full neurorestorative program in PD. Full article
(This article belongs to the Special Issue Neuron Cell Death)
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18 pages, 261 KiB  
Review
Neuronal Cell Death Mechanisms in Major Neurodegenerative Diseases
by Hao Chi, Hui-Yun Chang and Tzu-Kang Sang
Int. J. Mol. Sci. 2018, 19(10), 3082; https://doi.org/10.3390/ijms19103082 - 09 Oct 2018
Cited by 215 | Viewed by 24138
Abstract
Neuronal cell death in the central nervous system has always been a challenging process to decipher. In normal physiological conditions, neuronal cell death is restricted in the adult brain, even in aged individuals. However, in the pathological conditions of various neurodegenerative diseases, cell [...] Read more.
Neuronal cell death in the central nervous system has always been a challenging process to decipher. In normal physiological conditions, neuronal cell death is restricted in the adult brain, even in aged individuals. However, in the pathological conditions of various neurodegenerative diseases, cell death and shrinkage in a specific region of the brain represent a fundamental pathological feature across different neurodegenerative diseases. In this review, we will briefly go through the general pathways of cell death and describe evidence for cell death in the context of individual common neurodegenerative diseases, discussing our current understanding of cell death by connecting with renowned pathogenic proteins, including Tau, amyloid-beta, alpha-synuclein, huntingtin and TDP-43. Full article
(This article belongs to the Special Issue Neuron Cell Death)
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12 pages, 487 KiB  
Review
Alcohol and the Developing Brain: Why Neurons Die and How Survivors Change
by Alberto Granato and Benjamin Dering
Int. J. Mol. Sci. 2018, 19(10), 2992; https://doi.org/10.3390/ijms19102992 - 30 Sep 2018
Cited by 28 | Viewed by 7579
Abstract
The consequences of alcohol drinking during pregnancy are dramatic and usually referred to as fetal alcohol spectrum disorders (FASD). This condition is one of the main causes of intellectual disability in Western countries. The immature fetal brain exposed to ethanol undergoes massive neuron [...] Read more.
The consequences of alcohol drinking during pregnancy are dramatic and usually referred to as fetal alcohol spectrum disorders (FASD). This condition is one of the main causes of intellectual disability in Western countries. The immature fetal brain exposed to ethanol undergoes massive neuron death. However, the same mechanisms leading to cell death can also be responsible for changes of developmental plasticity. As a consequence of such a maladaptive plasticity, the functional damage to central nervous system structures is amplified and leads to permanent sequelae. Here we review the literature dealing with experimental FASD, focusing on the alterations of the cerebral cortex. We propose that the reciprocal interaction between cell death and maladaptive plasticity represents the main pathogenetic mechanism of the alcohol-induced damage to the developing brain. Full article
(This article belongs to the Special Issue Neuron Cell Death)
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17 pages, 1087 KiB  
Review
Molecular Communication of a Dying Neuron in Stroke
by Berta Puig, Santra Brenna and Tim Magnus
Int. J. Mol. Sci. 2018, 19(9), 2834; https://doi.org/10.3390/ijms19092834 - 19 Sep 2018
Cited by 90 | Viewed by 9189
Abstract
When a main artery of the brain occludes, a cellular response involving multiple cell types follows. Cells directly affected by the lack of glucose and oxygen in the neuronal core die by necrosis. In the periphery surrounding the ischemic core (the so-called penumbra) [...] Read more.
When a main artery of the brain occludes, a cellular response involving multiple cell types follows. Cells directly affected by the lack of glucose and oxygen in the neuronal core die by necrosis. In the periphery surrounding the ischemic core (the so-called penumbra) neurons, astrocytes, microglia, oligodendrocytes, pericytes, and endothelial cells react to detrimental factors such as excitotoxicity, oxidative stress, and inflammation in different ways. The fate of the neurons in this area is multifactorial, and communication between all the players is important for survival. This review focuses on the latest research relating to synaptic loss and the release of apoptotic bodies and other extracellular vesicles for cellular communication in stroke. We also point out possible treatment options related to increasing neuronal survival and regeneration in the penumbra. Full article
(This article belongs to the Special Issue Neuron Cell Death)
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49 pages, 1286 KiB  
Review
Unraveling the Pathways to Neuronal Homeostasis and Disease: Mechanistic Insights into the Role of RNA-Binding Proteins and Associated Factors
by Stylianos Ravanidis, Fedon-Giasin Kattan and Epaminondas Doxakis
Int. J. Mol. Sci. 2018, 19(8), 2280; https://doi.org/10.3390/ijms19082280 - 03 Aug 2018
Cited by 40 | Viewed by 9683
Abstract
The timing, dosage and location of gene expression are fundamental determinants of brain architectural complexity. In neurons, this is, primarily, achieved by specific sets of trans-acting RNA-binding proteins (RBPs) and their associated factors that bind to specific cis elements throughout the RNA sequence [...] Read more.
The timing, dosage and location of gene expression are fundamental determinants of brain architectural complexity. In neurons, this is, primarily, achieved by specific sets of trans-acting RNA-binding proteins (RBPs) and their associated factors that bind to specific cis elements throughout the RNA sequence to regulate splicing, polyadenylation, stability, transport and localized translation at both axons and dendrites. Not surprisingly, misregulation of RBP expression or disruption of its function due to mutations or sequestration into nuclear or cytoplasmic inclusions have been linked to the pathogenesis of several neuropsychiatric and neurodegenerative disorders such as fragile-X syndrome, autism spectrum disorders, spinal muscular atrophy, amyotrophic lateral sclerosis and frontotemporal dementia. This review discusses the roles of Pumilio, Staufen, IGF2BP, FMRP, Sam68, CPEB, NOVA, ELAVL, SMN, TDP43, FUS, TAF15, and TIA1/TIAR in RNA metabolism by analyzing their specific molecular and cellular function, the neurological symptoms associated with their perturbation, and their axodendritic transport/localization along with their target mRNAs as part of larger macromolecular complexes termed ribonucleoprotein (RNP) granules. Full article
(This article belongs to the Special Issue Neuron Cell Death)
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20 pages, 2800 KiB  
Review
Heme Oxygenase 1 in the Nervous System: Does It Favor Neuronal Cell Survival or Induce Neurodegeneration?
by Mariapaola Nitti, Sabrina Piras, Lorenzo Brondolo, Umberto Maria Marinari, Maria Adelaide Pronzato and Anna Lisa Furfaro
Int. J. Mol. Sci. 2018, 19(8), 2260; https://doi.org/10.3390/ijms19082260 - 01 Aug 2018
Cited by 107 | Viewed by 6299
Abstract
Heme oxygenase 1 (HO-1) up-regulation is recognized as a pivotal mechanism of cell adaptation to stress. Under control of different transcription factors but with a prominent role played by Nrf2, HO-1 induction is crucial also in nervous system response to damage. However, several [...] Read more.
Heme oxygenase 1 (HO-1) up-regulation is recognized as a pivotal mechanism of cell adaptation to stress. Under control of different transcription factors but with a prominent role played by Nrf2, HO-1 induction is crucial also in nervous system response to damage. However, several lines of evidence have highlighted that HO-1 expression is associated to neuronal damage and neurodegeneration especially in Alzheimer’s and Parkinson’s diseases. In this review, we summarize the current literature regarding the role of HO-1 in nervous system pointing out different molecular mechanisms possibly responsible for HO-1 up-regulation in nervous system homeostasis and neurodegeneration. Full article
(This article belongs to the Special Issue Neuron Cell Death)
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