ArticleJournal of burn care & research : official publication of the American Burn Association
Long-Term Skeletal Muscle Mitochondrial Dysfunction is Associated with Hypermetabolism in Severely Burned Children.
Article in Journal of burn care & research : official publication of the American Burn Association. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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The trial behind it
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Who cites it
31 citing papers in PubMed, 50 citations in OpenAlex.
- Skeletal Muscle Mitochondrial Function is Determined by Burn Severity, Sex, and Sepsis, and is Associated With Glucose Metabolism and Functional Capacity in Burned Children.Shock (Augusta, Ga.) · 2018Trial
- Short-term metformin and exercise training effects on strength, aerobic capacity, glycemic control, and mitochondrial function in children with burn injury.American journal of physiology. Endocrinology and metabolism · 2018Trial
- Mitochondria as a Therapeutic Target for Burn Injury.Biomolecules · 2026Review
- Effect of a 6-Week Structured Exercise Intervention on TNF-α During the Chronic Recovery Phase of a Burn Injury Compared to Regular Daily Activities: A Pilot Randomised Cross-Over Trial.European burn journal · 2026Article
- The short-term and long-term effect of burn on organ dysfunction: mechanisms and strategies.Frontiers in immunology · 2026Review
- The Role of Previous History of Muscle Wasting in Burn Outcomes-A Burn Care Quality Platform Study.European burn journal · 2025Article
- Metabolic and Hormonal Changes in Pediatric Burn Patients: Mechanisms, Evidence, and Care Strategies.European burn journal · 2025Review
- Activated Microglia Mediate the Motor Neuron-, Synaptic Denervation- and Muscle Wasting-Changes in Burn Injured Mice.Journal of cachexia, sarcopenia and muscle · 2025Article
- Farnesysltransferase Inhibitor Prevents Burn Injury-Induced Metabolome Changes in Muscle.Metabolites · 2022Article
- [A brief discussion on precision nutrition support for severe burn patients from theory to practice].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2022Article
- Burn-induced hypermetabolism and skeletal muscle dysfunction.American journal of physiology. Cell physiology · 2021Review
- The impact of catecholamines on skeletal muscle following massive burns: Friend or foe?Burns : journal of the International Society for Burn Injuries · 2021Review
- ASCs derived from burn patients are more prone to increased oxidative metabolism and reactive oxygen species upon passaging.Stem cell research & therapy · 2021Article
- Mitochondria-cytokine crosstalk following skeletal muscle injury and disuse: a mini-review.American journal of physiology. Cell physiology · 2021Review
- The pathogenesis and diagnosis of sepsis post burn injury.Burns & trauma · 2021Review
- Increased oxidative phosphorylation in lymphocytes does not atone for decreased cell numbers after burn injury.Innate immunity · 2020Article
- Burn-Induced Cardiac Mitochondrial Dysfunction via Interruption of the PDE5A-cGMP-PKG Pathway.International journal of molecular sciences · 2020Article
- Erythropoietin Alleviates Burn-induced Muscle Wasting.International journal of medical sciences · 2020Article
- Determinants of skeletal muscle protein turnover following severe burn trauma in children.Clinical nutrition (Edinburgh, Scotland) · 2019Observational
- Understanding acute burn injury as a chronic disease.Burns & trauma · 2019Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
The long-term impact of burn trauma on skeletal muscle bioenergetics remains unknown. Here, the authors determined respiratory capacity and function of skeletal muscle mitochondria in healthy individuals and in burn victims for up to 2 years postinjury. Biopsies were collected from the m. vastus lateralis of 16 healthy men (26 ± 4 years) and 69 children (8 ± 5 years) with burns encompassing ≥30% of their total BSA. Seventy-nine biopsies were collected from cohorts of burn victims at 2 weeks (n = 18), 6 months (n = 18), 12 months (n = 25), and 24 months (n = 18) postburn. Hypermetabolism was determined by the difference in predicted and measured metabolic rate. Mitochondrial respiration was determined in saponin-permeabilized myofiber bundles. Outcomes were modeled by analysis of variance, with differences in groups assessed by Tukey-adjusted contrasts. Burn patients were hypermetabolic for up to 2 years postinjury. Coupled mitochondrial respiration was lower at 2 weeks (17 [8] pmol/sec/mg; P < .001), 6 months (41 [30] pmol/sec/mg; P = .03), and 12 months (35 [14] pmol/sec/mg; P < .001) postburn compared with healthy controls (58 [13] pmol/sec/mg). Coupled respiration was greater at 6, 12, and 24 months postburn vs 2 weeks postburn (P < .001). Mitochondrial adenosine diphosphate and oligomycin sensitivity (measures of coupling control) were lower at all time-points postburn vs control (P < .05), but greater at 6, 12, and 24 months postburn vs 2 weeks postburn (P < .05). Muscle mitochondrial respiratory capacity remains significantly lower in burn victims for 1-year postinjury. Mitochondrial coupling control is diminished for up to 2 years postinjury in burn victims, resulting in greater mitochondrial thermogenesis. These quantitative and qualitative derangements in skeletal muscle bioenergetics likely contribute to the long-term pathophysiological stress response to burn trauma.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.