Metabolic Responses and Recovery Strategies in Burn Injuries

Severe burn injury triggers a profound systemic reaction characterised by an immediate hypermetabolic state, extensive protein catabolism and a sustained hyperinflammatory response. The loss of skin integrity leads to massive fluid, electrolyte and heat losses that drive endocrine alterations, including elevated catecholamines, cortisol and inflammatory cytokines. These hormonal changes fuel gluconeogenesis, lipolysis and proteolysis, resulting in muscle wasting and impaired organ function. The liver assumes a pivotal role in orchestrating metabolic and acute phase responses, yet is itself vulnerable to burn‐induced damage, particularly in aged individuals. Meanwhile, mitochondrial dysfunction and oxidative stress contribute to long‐term organ derangements in heart, lung and skeletal muscle. Nutritional support, alongside pharmacological modulation of stress mediators, forms the cornerstone of recovery strategies. Early enteral feeding with high‐carbohydrate formulations aims to meet the elevated energy demand, while agents such as nonselective β-blockers and histamine H1 receptor antagonists are under investigation for attenuation of the catecholamine surge and organ protection. Biomaterial‐based dressings and tissue‐engineered grafts further complement systemic therapies by optimising local wound healing. A combined approach that integrates molecular insights, personalised nutrition and targeted therapeutics is essential to improve outcomes and reduce long‐term morbidity following burn injury.

Research from Nature Portfolio

A comprehensive multi-omics investigation examined age-specific hepatic responses to burn injury in murine models. By integrating transcriptomic and metabolomic profiles of young and aged livers, the study delineated differential activation of master regulators and metabolic pathways that underlie heightened vulnerability in older animals. Computational drug-target prediction highlighted potential small molecules capable of mitigating burn-induced hepatic injury by restoring dysregulated pathways. This work provides a blueprint for precision therapies aimed at organ-specific protection and reveals how age modifies systemic metabolic adaptation after severe thermal trauma.

Metabolic Responses and Recovery Strategies in Burn Injuries publication trend

The graph below shows the total number of articles in metabolic responses and recovery strategies in burn injuries across all publications each year (not limited to Nature Index journals).

Technical terms

Hypermetabolism: A sustained increase in resting energy expenditure following burn injury, driven by hormonal and inflammatory mediators.

Catabolism: The breakdown of complex molecules such as proteins and fats into simpler compounds, leading to muscle wasting and energy production.

Acute phase response: A rapid systemic reaction to injury or infection marked by altered production of plasma proteins by the liver, including inflammatory mediators.

Gluconeogenesis: The metabolic pathway by which glucose is synthesised from non‐carbohydrate precursors, typically upregulated in burn-induced stress.

Transcriptomics: The large-scale study of RNA transcripts produced by the genome under specific conditions, used to reveal gene expression changes.

Metabolomics: The comprehensive analysis of small molecule metabolites within cells or tissues, used to map metabolic alterations after injury.

References

1. Transcriptomics, metabolomics, and in-silico drug predictions for liver damage in young and aged burn victims. Communications Biology (2023).
2. Burns: Classification, Pathophysiology, and Treatment: A Review. International Journal of Molecular Sciences (2023).
3. Histamine H1 receptor antagonist attenuates catecholamine surge and organ injury after severe burns. Frontiers in Endocrinology (2023).
4. The Hepatic Response to Thermal Injury: Is the Liver Important for Postburn Outcomes?. Molecular Medicine (2009).
5. Time-Dependent and Organ-Specific Changes in Mitochondrial Function, Mitochondrial DNA Integrity, Oxidative Stress and Mononuclear Cell Infiltration in a Mouse Model of Burn Injury. PLOS ONE (2015).
6. Propranolol attenuates hemorrhage and accelerates wound healing in severely burned adults. Critical Care (2015).