Key result
Expression of the SOD3 R213G variant in transgenic mice caused premature aging, systemic inflammation, and organ degeneration due to uncontrolled neutrophil-mediated reactive oxygen species.
Population
SOD3 R213G transgenic mice (variant gene driven by β-actin promoter)
Design
Preclinical
Authors
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May link SOD3 R213G to human inflammatory aging; leaves open translation from mouse models.
The SOD3 R213G variant leads to premature aging, systemic inflammation, and organ degeneration in mice due to altered ROS moderation in the extracellular matrix.
Kwon et al. (2015) studied Premature aging and systemic inflammation. SOD3 R213G transgenic expression was evaluated on Premature aging, systemic inflammation, and organ degeneration. Expression of the SOD3 R213G variant in transgenic mice caused premature aging, systemic inflammation, and organ degeneration due to uncontrolled neutrophil-mediated reactive oxygen species.
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