Research identifies mitochondria as key to treating severe burns, suggesting new pharmacological strategies.
Severe burn injury results in systemic inflammation, edema, multiple organ disorder and muscle wasting. These events are provoked by the massive dysfunction of mitochondria not only in the burned skin but also in muscles and internal organs, which is induced by the release of damage-associated molecular patterns and catecholamines. Dysfunctional mitochondria are characterized by increased ROS production and the release of mitochondrial DNA, which lead to enhanced expression of proinflammatory cytokines. Mitochondria present a key target for treatment of severe burns, and various pharmacological approaches are being developed to protect normal mitochondrial functions after burn injury.
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Prudovsky et al. (2026) studied this question.
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