ArticleCell death & disease2019
Browning of white adipose tissue after a burn injury promotes hepatic steatosis and dysfunction.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 61 citations in OpenAlex.
- Review
- HSF1 inhibits smooth muscle gene program to enhance white fat browning and hypermetabolism after burn injury.Science China. Life sciences · 2026Article
- Experimental sepsis causes SERCA2 expression in white adipose tissue but not classical browning.Scientific reports · 2026Article
- Adipocytes influence choroidal neovascularization via PRDM16.EMBO molecular medicine · 2026Article
- Burn-associated metabolic dysfunction: could extracellular vesicles play a role?Clinical science (London, England : 1979) · 2026Review
- Mitochondria as a Therapeutic Target for Burn Injury.Biomolecules · 2026Review
- Dynamic Lipidomic Responses to Inflammation and Physical Insult: A Comparative Review Across Blunt Force Trauma, Thermal Burn Injury, and Viral Infection.Expert reviews in molecular medicine · 2026Review
- Cancer cachexia: molecular basis and therapeutic advances.Signal transduction and targeted therapy · 2026Review
- Hypermetabolism and Lipid Alterations Postburn: A Cardiovascular Perspective.Cardiovascular therapeutics · 2026Review
- Burns: The "Fuse" That Ignites Organ Crisis - A Narrative Review of Mechanisms and Crosstalk in Post-Burn MODS.Journal of inflammation research · 2026Review
- Dermorphin [D-Arg2, Lys4] (1-4) Amide Attenuates Burn Pain by Inhibiting TRPV1/NR2B Mediated Neuroinflammatory Signalling.Molecular neurobiology · 2025Article
- The flux of energy in critical illness and the obesity paradox.Physiological reviews · 2025Review
- Radiation Promotes Acute and Chronic Damage to Adipose Tissue.International journal of molecular sciences · 2025Article
- Metabolic and Hormonal Changes in Pediatric Burn Patients: Mechanisms, Evidence, and Care Strategies.European burn journal · 2025Review
- Study on metabolic disorders in rat liver induced by different times after scalds.Biochemistry and biophysics reports · 2025Article
- The Different Shades of Thermogenic Adipose Tissue.Current obesity reports · 2024Review
- Nonsevere Burn Induces a Prolonged Systemic Metabolic Phenotype Indicative of a Persistent Inflammatory Response Postinjury.Journal of proteome research · 2024Article
- Subcutaneous white adipose tissue independently regulates burn-induced hypermetabolism via immune-adipose crosstalk.Cell reports · 2024Article
- Hyperactive browning and hypermetabolism: potentially dangerous element in critical illness.Frontiers in endocrinology · 2024Review
- Burn-Induced Apoptosis in the Livers of Aged Mice Is Associated With Caspase Cleavage of Bcl-xL.The Journal of surgical research · 2023Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
Abstract
Burn patients experiencing hypermetabolism develop hepatic steatosis, which is associated with liver failure and poor outcomes after the injury. These same patients also undergo white adipose tissue (WAT) browning, which has been implicated in mediating post-burn cachexia and sustained hypermetabolism. Despite the clinical presentation of hepatic steatosis and WAT browning in burns, whether or not these two pathological responses are linked remains poorly understood. Here, we show that the burn-induced WAT browning and its associated increased lipolysis leads to the accelerated development of hepatic steatosis in mice. Deletion of interleukin 6 (IL-6) and the uncoupling protein 1 (UCP1), regulators of burn-induced WAT browning completely protected mice from hepatic steatosis after the injury. Treatment of post-burn mice with propranolol or IL-6 receptor blocker attenuated burn-induced WAT browning and its associated hepatic steatosis pathology. Lipidomic profiling in the plasma of post-burn mice and burn patients revealed elevated levels of damage-inducing lipids (palmitic and stearic acids), which induced hepatic endoplasmic reticulum (ER) stress and compromised hepatic fat oxidation. Mechanistically, we show that hepatic ER stress after a burn injury leads to a greater ER-mitochondria interaction, hepatocyte apoptosis, oxidative stress, and impaired fat oxidation. Collectively, our findings uncover an adverse "cross-talk" between the adipose and liver tissue in the context of burn injury, which is critically mediated by WAT browning.
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Registered trials
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