ArticleShock (Augusta, Ga.)2018
Burn Trauma Acutely Increases the Respiratory Capacity and Function of Liver Mitochondria.
Article in Shock (Augusta, Ga.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Mitochondria as a Therapeutic Target for Burn Injury.Biomolecules · 2026Review
- Burns: The "Fuse" That Ignites Organ Crisis - A Narrative Review of Mechanisms and Crosstalk in Post-Burn MODS.Journal of inflammation research · 2026Review
- Burn-induced mitochondrial dysfunction in hepatocytes: The role of methylation-controlled J protein silencing.The journal of trauma and acute care surgery · 2025Article
- HOUSING TEMPERATURE ALTERS BURN-INDUCED HYPERMETABOLISM IN MICE.Shock (Augusta, Ga.) · 2025Article
- Glutamine sustains energy metabolism and alleviates liver injury in burn sepsis by promoting the assembly of mitochondrial HSP60-HSP10 complex via SIRT4 dependent protein deacetylation.Redox report : communications in free radical research · 2024Article
- Murine scald models characterize the role of neutrophils and neutrophil extracellular traps in severe burns.Frontiers in immunology · 2023Article
- Effect of Mitochondrial Antioxidant (Mito-TEMPO) on Burn-Induced Cardiac Dysfunction.Journal of the American College of Surgeons · 2021Article
- The Genetic Evidence of Burn-Induced Cardiac Mitochondrial Metabolism Dysfunction.Biomedicines · 2020Article
- Brown adipose tissue recruitment in a rodent model of severe burns.Burns : journal of the International Society for Burn Injuries · 2020Article
- Sildenafil Recovers Burn-Induced Cardiomyopathy.Cells · 2020Article
- Cardiac Dysfunction after Burn Injury: Role of the AMPK-SIRT1-PGC1α-NFE2L2-ARE Pathway.Journal of the American College of Surgeons · 2020Article
- Burn-Induced Cardiac Mitochondrial Dysfunction via Interruption of the PDE5A-cGMP-PKG Pathway.International journal of molecular sciences · 2020Article
- Burn-Induced Impairment of Ileal Muscle Contractility Is Associated with Increased Extracellular Matrix Components.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2020Article
- Regulation of Mitochondrial Biogenesis as a Way for Active Longevity: Interaction Between the Nrf2 and PGC-1α Signaling Pathways.Frontiers in genetics · 2019Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundA complete understanding of the role of the liver in burn-induced hypermetabolism is lacking. We investigated the acute effect of severe burn trauma on liver mitochondrial respiratory capacity and coupling control as well as the signaling events underlying these alterations.
methodsMale BALB/c mice (8-12 weeks) received full-thickness scald burns on ∼30% of the body surface. Liver tissue was harvested 24 h postinjury. Mitochondrial respiration was determined by high-resolution respirometry. Citrate synthase activity was determined as a proxy of mitochondrial density. Male Sprague-Dawley rats received full-thickness scald burns to ∼60% of the body surface. Serum was collected 24 h postinjury. HepG2 cells were cultured with serum-enriched media from either sham- or burn-treated rats. Protein levels were analyzed via western blot.
resultsMass-specific (P = 0.01) and mitochondrial-specific (P = 0.01) respiration coupled to ATP production significantly increased in the liver after burn. The respiratory control ratio for ADP (P = 0.04) and the mitochondrial flux control ratio (P = 0.03) were elevated in the liver of burned animals. Complex III and Complex IV protein abundance in the liver increased after burn by 17% and 14%, respectively. Exposure of HepG2 cells to serum from burned rats increased the pAMPKα:AMPKα ratio (P < 0.001) and levels of SIRT1 (P = 0.01), Nrf2 (P < 0.001), and PGC1α (P = 0.02).
conclusionsSevere burn trauma augments respiratory capacity and function of liver mitochondria, adaptations that augment ATP production. This response may be mediated by systemic factors that activate signaling proteins responsible for regulating cellular energy metabolism and mitochondrial biogenesis.
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Registered trials
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