What is it about?
The oxidative stress enzyme NADPH oxidase (NOX) has a number of isoforms, including NOX2 and NOX4. Both are increased after spinal cord injury in animal models. We aimed to determine if both contribute to poor outcomes after injury by knocking out expression of NOX2 or using a drug to inhibit the activity of NOX4. We found that knockout of NOX2 improved outcome after spinal cord injury in mice, by reducing post-injury inflammation and oxidative stress. However, while inhibiting NOX4 activity reduced some aspects of inflammation and acute oxidative stress, it did not result in long-term functional improvements. Therefore, both NOX2 and NOX4 play a role in post-injury inflammation and oxidative stress, but NOX2 may be a more viable therapeutic target for spinal cord injury.
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Why is it important?
To determine good therapeutic approaches for spinal cord injury, understanding of the components of injury is important.
Perspectives
Our previous work showed that a drug that blocked NOX2 function also improved functional recovery; this finding in the genetic knockout shows that the drug effects and the genetic effects are very similar. At the same time, we show that targeting another NOX isoform is less effective in reducing post-injury impairments.
Kimberly Byrnes
Uniformed Services University
Read the Original
This page is a summary of: Differential effects of NOX2 and NOX4 inhibition after rodent spinal cord injury, PLOS One, March 2023, PLOS,
DOI: 10.1371/journal.pone.0281045.
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