ArticleBiochimica et biophysica acta. Molecular basis of disease2017
Hepatic mitochondrial bioenergetics in aged C57BL/6 mice exhibit delayed recovery from severe burn injury.
Article in Biochimica et biophysica acta. Molecular basis of disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Mitochondria as a Therapeutic Target for Burn Injury.Biomolecules · 2026Review
- Article
- Hepatocyte Mitochondrial Dynamics and Bioenergetics in Obesity-Related Non-Alcoholic Fatty Liver Disease.Current obesity reports · 2022Review
- Adipose browning response to burn trauma is impaired with aging.JCI insight · 2021Observational
- Burn-induced hypermetabolism and skeletal muscle dysfunction.American journal of physiology. Cell physiology · 2021Review
- Adipose-specific ATGL ablation reduces burn injury-induced metabolic derangements in mice.Clinical and translational medicine · 2021Article
- Pathological Responses of Cardiac Mitochondria to Burn Trauma.International journal of molecular sciences · 2020Review
- Increased proliferation of hepatic periportal ductal progenitor cells contributes to persistent hypermetabolism after trauma.Journal of cellular and molecular medicine · 2020Article
- Metformin prevents the pathological browning of subcutaneous white adipose tissue.Molecular metabolism · 2019Article
- Modelling physical resilience in ageing mice.Mechanisms of ageing and development · 2019Review
- Hepatic steatosis associated with decreased β-oxidation and mitochondrial function contributes to cell damage in obese mice after thermal injury.Cell death & disease · 2018Article
- Metformin adapts its cellular effects to bioenergetic status in a model of metabolic dysfunction.Scientific reports · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Severe burn injuries initiate a cascade of downstream events, culminating in multiple organ dysfunction, sepsis, and even death. The elderly are in particular vulnerable to such outcomes, due primarily to a scarcity of knowledge on trauma progression at the biomolecular level in this population. Mitochondria, the cellular powerhouses, have been increasingly scrutinized recently for their contribution to trauma outcomes. We hypothesized that elderly have a worse outcome compared to adult patients due to failed recovery of hepatic mitochondria. Using a murine model of burn injury, Seahorse respirometry and functional proteomic assays, we demonstrate the impact of thermal trauma on hepatic mitochondrial respiration in adult and aged mice. While the mitochondria in adults rebound from the initial insult within 7days of the injury, the older animals display delayed recovery of mitochondrial bioenergetics accompanied by uncoupling and an oxidative environment. This is associated with a state of increased protein oxidation and nitrosylation, along with increases in circulating mtDNA, a known damage-associated molecular pattern. These findings suggest that hepatic mitochondria fail to normalize after trauma in aged mice and we suggest that this cellular failure is associated with organ damage and subsequently increased morbidity and mortality in elderly burn patients.
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