ArticleScientific reports2017
Burn-induced muscle metabolic derangements and mitochondrial dysfunction are associated with activation of HIF-1α and mTORC1: Role of protein farnesylation.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- [Research progress on the roles of mitochondrial fusion, fission, and mitophagy in burn wound healing].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026Review
- Optical, Tomographic, and Mass Spectrometry Imaging Methods for Burn Wounds: Capabilities, Limitations, and Clinical Potential.Biomedicines · 2026Review
- Mitochondria as a Therapeutic Target for Burn Injury.Biomolecules · 2026Review
- Insulin Resistance and Inflammation.International journal of molecular sciences · 2026Review
- The worsening of skeletal muscle atrophy induced by immobilization at the early stage of remobilization correlates with BNIP3-dependent mitophagy.BMC musculoskeletal disorders · 2023Article
- [Application and research progress of permissive hypocaloric nutrition in nutritional therapy of severe burns].Zhonghua shao shang yu chuang mian xiu fu za zhi · 2023Article
- Potential Role of the mTORC1-PGC1α-PPARα Axis under Type-II Diabetes and Hypertension in the Human Heart.International journal of molecular sciences · 2023Article
- Mitochondrial dysfunction and mitophagy: crucial players in burn trauma and wound healing.Burns & trauma · 2023Review
- Spinal Irisin Gene Delivery Attenuates Burn Injury-Induced Muscle Atrophy by Promoting Axonal Myelination and Innervation of Neuromuscular Junctions.International journal of molecular sciences · 2022Article
- Farnesysltransferase Inhibitor Prevents Burn Injury-Induced Metabolome Changes in Muscle.Metabolites · 2022Article
- C188-9, a specific inhibitor of STAT3 signaling, prevents thermal burn-induced skeletal muscle wasting in mice.Frontiers in pharmacology · 2022Article
- Burn-induced hypermetabolism and skeletal muscle dysfunction.American journal of physiology. Cell physiology · 2021Review
- Canagliflozin attenuates lipotoxicity in cardiomyocytes and protects diabetic mouse hearts by inhibiting the mTOR/HIF-1α pathway.iScience · 2021Article
- Protective effects of farnesyltransferase inhibitor on sepsis-induced morphological aberrations of mitochondria in muscle and increased circulating mitochondrial DNA levels in mice.Biochemical and biophysical research communications · 2021Article
- Myostatin deficiency not only prevents muscle wasting but also improves survival in septic mice.American journal of physiology. Endocrinology and metabolism · 2021Article
- Hyperbaric Oxygen Therapy Attenuates Burn-Induced Denervated Muscle Atrophy.International journal of medical sciences · 2021Article
- The Genetic Evidence of Burn-Induced Cardiac Mitochondrial Metabolism Dysfunction.Biomedicines · 2020Article
- Article
- Coenzyme Q10 protects against burn-induced mitochondrial dysfunction and impaired insulin signaling in mouse skeletal muscle.FEBS open bio · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 7 institutions in 2 countries.
Funding
Abstract
Metabolic derangements are a clinically significant complication of major trauma (e.g., burn injury) and include various aspects of metabolism, such as insulin resistance, muscle wasting, mitochondrial dysfunction and hyperlactatemia. Nonetheless, the molecular pathogenesis and the relation between these diverse metabolic alterations are poorly understood. We have previously shown that burn increases farnesyltransferase (FTase) expression and protein farnesylation and that FTase inhibitor (FTI) prevents burn-induced hyperlactatemia, insulin resistance, and increased proteolysis in mouse skeletal muscle. In this study, we found that burn injury activated mTORC1 and hypoxia-inducible factor (HIF)-1α, which paralleled dysfunction, morphological alterations (i.e., enlargement, partial loss of cristae structure) and impairment of respiratory supercomplex assembly of the mitochondria, and ER stress. FTI reversed or ameliorated all of these alterations in burned mice. These findings indicate that these burn-induced changes, which encompass various aspects of metabolism, may be linked to one another and require protein farnesylation. Our results provide evidence of involvement of the mTORC1-HIF-1α pathway in burn-induced metabolic derangements. Our study identifies protein farnesylation as a potential hub of the signaling network affecting multiple aspects of metabolic alterations after burn injury and as a novel potential molecular target to improve the clinical outcome of severely burned patients.
Indexed as
Identifiers
What OpenQuestion holds
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.