Corpus ID: 201688083

Crosstalk between mitochondrial dysfunction and neuroinflammation in TBI

@inproceedings{Gu2018CrosstalkBM,
  title={Crosstalk between mitochondrial dysfunction and neuroinflammation in TBI},
  author={Zheng-tao Gu and Lingjiao Huang and Hong Yang and Ming Zhao},
  year={2018}
}
Traumatic brain injury (TBI) affects a growing population of all ages with long-term consequences on health and cognition. Mitochondrial dysfunction and neuroinflammation are two main factors contributing to secondary injury in TBI-associated brain damage, which can ultimately lead to secondary cell death, neurodegeneration, and long-lasting neurological impairment. TBI can cause mitochondrial dysfunction and dynamic changes including reduced mitochondrial biogenesis, oxidative phosphorylation… Expand

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References

SHOWING 1-10 OF 167 REFERENCES
Evidence to support mitochondrial neuroprotection, in severe traumatic brain injury
TLDR
This review summarizes those aspects of mitochondrial dysfunction underlying TBI pathology with special attention to models of penetrating traumatic brain injury, an epidemic in modern American society. Expand
Mitochondria in traumatic brain injury and mitochondrial‐targeted multipotential therapeutic strategies
TLDR
Preclinical and clinical results of mitochondria‐targeted therapy show promise and mitochondrial‐ targeted multipotential therapeutic strategies offer new hope for the successful treatment of TBI and other acute brain injuries. Expand
SIRT1 plays a neuroprotective role in traumatic brain injury in rats via inhibiting the p38 MAPK pathway
TLDR
The 12 h after TBI may be a crucial time at which secondary damage occurs; the activation of SIRT1 expression and inhibition of the p38 MAPK pathway may play a neuroprotective role in preventing secondary damage post-TBI. Expand
Interactions of Oxidative Stress and Neurovascular Inflammation in the Pathogenesis of Traumatic Brain Injury
TLDR
The role of oxidative stress in TBI-mediated secondary damages is addressed by affecting the function of the vascular unit, changes in blood-brain barrier (BBB) permeability, posttraumatic edema formation, and modulation of various pathophysiological factors such as inflammatory factors and enzymes associated with trauma. Expand
Mitochondrial dysfunction and the inflammatory response.
TLDR
Strategies aimed at controlling excessive oxidative stress within mitochondria may represent both preventive and therapeutic interventions in inflammation. Expand
Transiently lowering tumor necrosis factor-α synthesis ameliorates neuronal cell loss and cognitive impairments induced by minimal traumatic brain injury in mice
TLDR
It is suggested that pharmacologically limiting the generation of TNF-α post mTBI may mitigate secondary brain damage and define a time-dependent window of up to 12 h to achieve this reversal. Expand
Interleukin 6 Mediates Neuroinflammation and Motor Coordination Deficits After Mild Traumatic Brain Injury and Brief Hypoxia in Mice
TLDR
The effects of brief hypoxia on mild TBI and whether IL-6 played a role in the neuroinflammatory and functional deficits after injury suggest that systemic IL- 6 modulates the degree of neuroinflammation and contributes to reduced motor coordination after Mild TBI. Expand
The p38α MAPK Regulates Microglial Responsiveness to Diffuse Traumatic Brain Injury
TLDR
Data suggest that p38α balances the inflammatory response by acutely attenuating the early proinflammatory cytokine surge while perpetuating the chronic microglia activation after TBI. Expand
Sigma-1 Receptor Modulates Neuroinflammation After Traumatic Brain Injury
TLDR
Sigma-1 receptors play a major role in inflammatory response after TBI and may serve as useful target for TBI treatment in the future. Expand
Inflammation and neuroprotection in traumatic brain injury.
TLDR
Known inflammatory mechanisms in TBI are reviewed to highlight clinical trials and neuroprotective therapeutic manipulations of pathologic and inflammatory mechanisms of TBI and to highlight promising therapeutic approaches now under pre-clinical development. Expand
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