ArticleJournal of cellular and molecular medicine2009
Calcium and ER stress mediate hepatic apoptosis after burn injury.
Article in Journal of cellular and molecular medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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The trial behind it
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Who cites it
54 citing papers in PubMed, 82 citations in OpenAlex.
- Occurrence of multiorgan dysfunction in pediatric burn patients: incidence and clinical outcome.Annals of surgery · 2014Trial
- Glucose control in severely thermally injured pediatric patients: what glucose range should be the target?Annals of surgery · 2010Trial
- Intensive insulin therapy in severely burned pediatric patients: a prospective randomized trial.American journal of respiratory and critical care medicine · 2010Trial
- Vancomycin population pharmacokinetics in patients with burns.Frontiers in medicine · 2026Article
- Potential Application of Plant-Derived Extracellular Vesicles in Treatment of Burn Wounds.International journal of nanomedicine · 2026Review
- Optimized Protocol for Primary Rat Hepatocyte Isolation and a Model for Investigating Experimental Steatosis.Methods and protocols · 2025Article
- Estradiol Alleviates Elevated Temperature-Induced Damage in Yak Oviductal Epithelial Cells by Maintaining Endoplasmic Reticulum Calcium Homeostasis.Animals : an open access journal from MDPI · 2025Article
- Burn-induced mitochondrial dysfunction in hepatocytes: The role of methylation-controlled J protein silencing.The journal of trauma and acute care surgery · 2025Article
- Burn-Induced Apoptosis in the Livers of Aged Mice Is Associated With Caspase Cleavage of Bcl-xL.The Journal of surgical research · 2023Article
- The molecular mechanism of GADD153 in apoptosis of keloid fibroblasts exposed to botulinum toxin type A.Journal of cellular and molecular medicine · 2021Article
- Burn-induced hypermetabolism and skeletal muscle dysfunction.American journal of physiology. Cell physiology · 2021Review
- Investigation of the effect of hyperthyroidism on endoplasmic reticulum stress and tran- sient receptor potential canonical 1 channel in the kidneyTurkish journal of medical sciences · 2021Article
- Glucose Metabolism in Burns-What Happens?International journal of molecular sciences · 2021Review
- Calcium Channels: Noteworthy Regulators and Therapeutic Targets in Dermatological Diseases.Frontiers in pharmacology · 2021Review
- Burn injury.Nature reviews. Disease primers · 2020Review
- Increased proliferation of hepatic periportal ductal progenitor cells contributes to persistent hypermetabolism after trauma.Journal of cellular and molecular medicine · 2020Article
- Ginsenoside Rk1 inhibits cell proliferation and promotes apoptosis in lung squamous cell carcinoma by calcium signaling pathway.RSC advances · 2019Article
- TRPC1 expression and function inhibit ER stress and cell death in salivary gland cells.FASEB bioAdvances · 2019Article
- Aggregated and Hyperstable Damage-Associated Molecular Patterns Are Released During ER Stress to Modulate Immune Function.Frontiers in cell and developmental biology · 2019Article
- Autophagy mediated by endoplasmic reticulum stress enhances the caffeine-induced apoptosis of hepatic stellate cells.International journal of molecular medicine · 2017Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
A hallmark of the disease state following severe burn injury is decreased liver function, which results in gross metabolic derangements that compromise patient survival. The underlying mechanisms leading to hepatocyte dysfunction after burn are essentially unknown. The aim of the present study was to determine the underlying mechanisms leading to hepatocyte dysfunction and apoptosis after burn. Rats were randomized to either control (no burn) or burn (60% total body surface area burn) and sacrificed at various time-points. Liver was either perfused to isolate primary rat hepatocytes, which were used for in vitro calcium imaging, or liver was harvested and processed for immunohistology, transmission electron microscopy, mitochondrial isolation, mass spectroscopy or Western blotting to determine the hepatic response to burn injury in vivo. We found that thermal injury leads to severely depleted endoplasmic reticulum (ER) calcium stores and consequent elevated cytosolic calcium concentrations in primary hepatocytes in vitro. Burn-induced ER calcium depletion caused depressed hepatocyte responsiveness to signalling molecules that regulate hepatic homeostasis, such as vasopressin and the purinergic agonist ATP. In vivo, thermal injury resulted in activation of the ER stress response and major alterations in mitochondrial structure and function - effects which may be mediated by increased calcium release by inositol 1,4,5-trisphosphate receptors. Our results reveal that thermal injury leads to dramatic hepatic disturbances in calcium homeostasis and resultant ER stress leading to mitochondrial abnormalities contributing to hepatic dysfunction and apoptosis after burn injury.
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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.