scholarly journals Extracellular Mitochondria Signals in CNS Disorders

2021 ◽  
Vol 9 ◽  
Author(s):  
Ji-Hyun Park ◽  
Kazuhide Hayakawa
Keyword(s):  
Energy Homeostasis ◽  
Critical Role ◽  
Neuronal Cell Death ◽  
Extracellular Fluid ◽  
Neuronal Cell ◽  
High Energy ◽  
Cns Disorders ◽  
Mitochondrial Transfer ◽  
The Central Nervous System

Mitochondria actively participate in the regulation of cell respiratory mechanisms, metabolic processes, and energy homeostasis in the central nervous system (CNS). Because of the requirement of high energy, neuronal functionality and viability are largely dependent on mitochondrial functionality. In the context of CNS disorders, disruptions of metabolic homeostasis caused by mitochondrial dysfunction lead to neuronal cell death and neuroinflammation. Therefore, restoring mitochondrial function becomes a primary therapeutic target. Recently, accumulating evidence suggests that active mitochondria are secreted into the extracellular fluid and potentially act as non-cell-autonomous signals in CNS pathophysiology. In this mini-review, we overview findings that implicate the presence of cell-free extracellular mitochondria and the critical role of intercellular mitochondrial transfer in various rodent models of CNS disorders. We also discuss isolated mitochondrial allograft as a novel therapeutic intervention for CNS disorders.

scholarly journals Role of Grina/Nmdara1 in the Central Nervous System Diseases

2020 ◽  
Vol 18 (9) ◽  
pp. 861-867
Author(s):  
Kai Chen ◽  
Liu Nan Yang ◽  
Chuan Lai ◽  
Dan Liu ◽  
Ling-Qiang Zhu
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neurological Diseases ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Human Beings ◽  
Major Depressive ◽  
The Central Nervous System ◽  
Underlying Mechanisms

Glutamate receptor, ionotropic, N-methyl-D-aspartate associated protein 1 (GRINA) is a member of the NMDA receptors (NMDARs) and is involved in several neurological diseases, which governs the key processes of neuronal cell death or the release of neurotransmitters. Upregulation of GRINA has been reported in multiple diseases in human beings, such as major depressive disorder (MDD) and schizophrenia (SCZ), with which the underlying mechanisms remain elusive. In this review, we provide a general overview of the expression and physiological function of GRINA in the central nervous system (CNS) diseases, including stroke, depression ,epilepsy, SCZ, and Alzheimer’s disease (AD).

scholarly journals A Critical Role of TRPM2 in Neuronal Cell Death by Hydrogen Peroxide

2006 ◽  
Vol 101 (1) ◽  
pp. 66-76 ◽  
Author(s):  
Shuji Kaneko ◽  
Seiko Kawakami ◽  
Yuji Hara ◽  
Minoru Wakamori ◽  
Etsuko Itoh ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Cell Death ◽  
Critical Role ◽  
Neuronal Cell Death ◽  
Neuronal Cell

scholarly journals JNK Pathway in CNS Pathologies

2021 ◽  
Vol 22 (8) ◽  
pp. 3883
Author(s):  
Teresa de los Reyes Corrales ◽  
María Losada-Pérez ◽  
Sergio Casas-Tintó
Keyword(s):  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Migration And Invasion ◽  
Jnk Pathway ◽  
Highly Active ◽  
Cell Tissue ◽  
Wide Range ◽  
The Central Nervous System ◽  
Stress Signals

The c-Jun N-terminal kinase (JNK) signalling pathway is a conserved response to a wide range of internal and external cellular stress signals. Beside the stress response, the JNK pathway is involved in a series of vital regulatory mechanisms during development and adulthood that are critical to maintain tissue homeostasis. These mechanisms include the regulation of apoptosis, growth, proliferation, differentiation, migration and invasion. The JNK pathway has a diverse functionality and cell-tissue specificity, and has emerged as a key player in regeneration, tumorigenesis and other pathologies. The JNK pathway is highly active in the central nervous system (CNS), and plays a central role when cells need to cope with pathophysiological insults during development and adulthood. Here, we review the implications of the JNK pathway in pathologies of the CNS. More specifically, we discuss some newly identified examples and mechanisms of JNK-driven tumor progression in glioblastoma, regeneration/repair after an injury, neurodegeneration and neuronal cell death. All these new discoveries support the central role of JNK in CNS pathologies and reinforce the idea of JNK as potential target to reduce their detrimental effects.

scholarly journals Chromosome Instability, Aging and Brain Diseases

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1256
Author(s):  
Ivan Y. Iourov ◽  
Yuri B. Yurov ◽  
Svetlana G. Vorsanova ◽  
Sergei I. Kutsev
Keyword(s):  
Brain Aging ◽  
Chromosome Instability ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Accelerated Aging ◽  
Brain Diseases ◽  
Aging Brain ◽  
Ontogenetic Changes ◽  
Health And Disease

Chromosome instability (CIN) has been repeatedly associated with aging and progeroid phenotypes. Moreover, brain-specific CIN seems to be an important element of pathogenic cascades leading to neurodegeneration in late adulthood. Alternatively, CIN and aneuploidy (chromosomal loss/gain) syndromes exhibit accelerated aging phenotypes. Molecularly, cellular senescence, which seems to be mediated by CIN and aneuploidy, is likely to contribute to brain aging in health and disease. However, there is no consensus about the occurrence of CIN in the aging brain. As a result, the role of CIN/somatic aneuploidy in normal and pathological brain aging is a matter of debate. Still, taking into account the effects of CIN on cellular homeostasis, the possibility of involvement in brain aging is highly likely. More importantly, the CIN contribution to neuronal cell death may be responsible for neurodegeneration and the aging-related deterioration of the brain. The loss of CIN-affected neurons probably underlies the contradiction between reports addressing ontogenetic changes of karyotypes within the aged brain. In future studies, the combination of single-cell visualization and whole-genome techniques with systems biology methods would certainly define the intrinsic role of CIN in the aging of the normal and diseased brain.

scholarly journals The essential role of sodium bioenergetics and ATP homeostasis in the developmental transitions of a cyanobacterium

2020 ◽  
Author(s):  
Sofia Doello ◽  
Markus Burkhardt ◽  
Karl Forchhammer
Keyword(s):  
Energy Homeostasis ◽  
Nitrogen Starvation ◽  
Critical Role ◽  
Quiescent State ◽  
Bacterial Survival ◽  
Bacterial Populations ◽  
Photoautotrophic Growth ◽  
Available Energy ◽  
Atp Levels

The ability to resume growth after a dormant period is an important strategy for the survival and spreading of bacterial populations. Energy homeostasis is critical in the transition into and out of a quiescent state. Synechocystis sp. PCC 6803, a non-diazotrophic cyanobacterium, enters metabolic dormancy as a response to nitrogen starvation. We used Synechocystis as a model to investigate the regulation of ATP homeostasis during dormancy and unraveled a critical role for sodium bioenergetics in dormant cells. During nitrogen starvation, cells reduce their ATP levels and engage sodium bioenergetics to maintain the minimum ATP content required for viability. When nitrogen becomes available, energy requirements rise, and cells immediately increase ATP levels employing sodium bioenergetics and glycogen catabolism. These processes allow them to restore the photosynthetic machinery and resume photoautotrophic growth. Our work reveals a precise regulation of the energy metabolism essential for bacterial survival during periods of nutrient deprivation.

The role of nitric oxide and PARP in neuronal cell death

2005 ◽  
pp. 146-156
Author(s):  
Mika Shimoji ◽  
Valina L. Dawson ◽  
Ted M. Dawson
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell
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