Traumatic brain injury and NADPH oxidase: a deep relationship.

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.

journal_name

Oxid Med Cell Longev

authors

Angeloni C,Prata C,Dalla Sega FV,Piperno R,Hrelia S

doi

10.1155/2015/370312

subject

Has Abstract

pub_date

2015-01-01 00:00:00

pages

370312

eissn

1942-0900

issn

1942-0994

journal_volume

2015

pub_type

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