Cited by 18Burn Injury Management and OutcomesMuscle Physiology and DisordersMitochondrial Function and Pathology

The Role of Mitochondrial Stress in Muscle Wasting Following Severe Burn Trauma

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Ogunbileje, John O, Herndon, David N, Murton, Andrew J, Porter, Craig·2017·Journal of Burn Care & Research

Abstract

Increased resting metabolic rate and skeletal muscle wasting are hallmarks of the pathophysiological stress response to severe burn trauma. However, whether these two responses occur independently in burn patients or are in fact related remains unclear. In light of recent evidence demonstrating that increased proteolysis in skeletal muscle of burned patients is accompanied by mitochondrial hypermetabolism, oxidative stress, and protein damage; in this article, we discuss the evidence for a role for the mitochondrion in skeletal muscle wasting following severe burn trauma. In particular, we focus on the role of mitochondrial superoxide production in oxidative stress and subsequent proteolysis, and discuss the role of the mitochondrion as a signaling organelle resulting in protein catabolism in other cellular compartments following severe burn trauma.

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  • Alterations in mitochondrial distribution, morphology, and function are present in atrophic muscles in aging, muscle disuse, burn injury, intensive care unit-acquired weakness, insulin resistance, chronic obstructive pulmonary disease, cancer cachexia, and different neuromuscular disorders.

    “Alterations in mitochondrial distribution, morphology, and function are present in atrophic muscles in aging [148–150], muscle disuse [151, 152], burn injury [153], intensive care unit-acquired weakness [154], insulin resistance [155] chronic obstructive pulmonary disease (COPD) [156], cancer cachexia [157–159], and different neuromuscular disorders [160].”

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  1. [54]Ogunbileje JO Porter C Herndon DN Chao T Abdelrahman DR Papadimitriou A Chondronikola M Zimmers TA Reidy PT Rasmussen BB Sidossis LS Hypermetabolism and hypercatabolism of skeletal muscle accompany mitochondrial stress following severe burn trauma American journal of physiology Endocrinology and metabolism 311 E436 448 2016 27382037 PMC5005969

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Authors
Ogunbileje, J. O., Herndon, D. N., Murton, A. J., & Porter, C.
Affiliations
Shriners Hospitals for Children - Galveston (US)
Corresponding author
Porter, Craig
Venue
Journal of Burn Care & Research
Published
2017-12-27
Volume
39
Issue
1
Pages
100-108
ISSN
  • 1559-047X (ISSN-L)
  • 1559-0488
OpenAlex
W2608634715
Cited by
18
References
82
Citations by year
2025: 3 · 2024: 1 · 2023: 2 · 2022: 4 · 2021: 1 · 2020: 4 · 2019: 1 · 2018: 1 · 2017: 1
FWCI
0.25
Type
journal article
Language
en
Open access
Locations
  • Journal of Burn Care & Research (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute of General Medical Sciences (P50GM060338, R01GM056687, T32GM008256)
Topics
  • Health Sciences › Medicine › Epidemiology › Burn Injury Management and Outcomes
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords
mitochondrial stress, skeletal muscle atrophy, mitochondrial superoxide, oxidative stress, muscle protein degradation, resting metabolic rate, mitochondrial signaling, protein degradation
MeSH terms
Basal Metabolism, Burns, Humans, Mitochondria, Muscular Atrophy, Superoxides, Oxidative Stress, Muscle, Skeletal

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