Mitochondria as a Therapeutic Target for Burn Injury

Document Type

Article

Publication Date

4-1-2026

Institution/Department

Center for Molecular Medicine

Journal Title

Biomolecules

MeSH Headings

Burns (metabolism, drug therapy, pathology); Humans; Mitochondria (metabolism, drug effects, pathology); Animals; Reactive Oxygen Species (metabolism); DNA, Mitochondrial (metabolism)

Abstract

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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