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Review
. 2015:2015:370312.
doi: 10.1155/2015/370312. Epub 2015 Mar 31.

Traumatic brain injury and NADPH oxidase: a deep relationship

Cristina Angeloni  1 , Cecilia Prata  2 , Francesco Vieceli Dalla Sega  2 , Roberto Piperno  3 , Silvana Hrelia  1
Affiliations
Review

Traumatic brain injury and NADPH oxidase: a deep relationship

Cristina Angeloni et al. Oxid Med Cell Longev. 2015.

Abstract

Traumatic brain injury (TBI) represents one of the major causes of mortality and disability in the world. TBI is characterized by primary damage resulting from the mechanical forces applied to the head as a direct result of the trauma and by the subsequent secondary injury due to a complex cascade of biochemical events that eventually lead to neuronal cell death. Oxidative stress plays a pivotal role in the genesis of the delayed harmful effects contributing to permanent damage. NADPH oxidases (Nox), ubiquitary membrane multisubunit enzymes whose unique function is the production of reactive oxygen species (ROS), have been shown to be a major source of ROS in the brain and to be involved in several neurological diseases. Emerging evidence demonstrates that Nox is upregulated after TBI, suggesting Nox critical role in the onset and development of this pathology. In this review, we summarize the current evidence about the role of Nox enzymes in the pathophysiology of TBI.

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Figures

Figure 1
Figure 1
Time related changes of Nox expression after TBI.
Figure 2
Figure 2
Schematic representation of the proposed mechanisms triggering cell damage after TBI.
See this image and copyright information in PMC

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