ArticleShock (Augusta, Ga.)2015
Lipopolysaccharide Disrupts Mitochondrial Physiology in Skeletal Muscle via Disparate Effects on Sphingolipid Metabolism.
Article in Shock (Augusta, Ga.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- The Skeletal Muscle as an Endocrine Firewall: Mitigating Metabolic Endotoxemia and Insulin Resistance in Polycystic Ovary Syndrome.Current obesity reports · 2026Review
- 2-Deoxy-D-Glucose restores glial cell mitochondrial function and attenuates neuroinflammation.Scientific reports · 2025Article
- Ceramides may Play a Central Role in the Pathogenesis of Alzheimer's Disease: a Review of Evidence and Horizons for Discovery.Molecular neurobiology · 2025Review
- Protective effects of enzymatically digested velvet antler polypeptides on mitochondria in primary astrocytes.Journal of animal science and technology · 2025Article
- The Role of Beta-Hydroxybutyrate in Mitigating the Inflammatory and Metabolic Consequences of Uric Acid.Metabolites · 2024Article
- Mitochondrial dysfunction in sepsis: mechanisms and therapeutic perspectives.Critical care (London, England) · 2024Review
- Endotoxin-induced alterations of adipose tissue function: a pathway to bovine metabolic stress.Journal of animal science and biotechnology · 2024Review
- Article
- Less Severe Polymicrobial Sepsis in ConditionalInternational journal of molecular sciences · 2023Article
- Zymosan-Induced Murine Peritonitis Is Associated with an Increased Sphingolipid Synthesis without Changing the Long to Very Long Chain Ceramide Ratio.International journal of molecular sciences · 2023Article
- Beta-Glucan fromInternational journal of molecular sciences · 2022Article
- Molecular Mechanisms Underlying Intensive Care Unit-Acquired Weakness and Sarcopenia.International journal of molecular sciences · 2022Review
- An Overview on Mitochondrial-Based Therapies in Sepsis-Related Myocardial Dysfunction: Mitochondrial Transplantation as a Promising Approach.The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2022Review
- TLR9 Signaling Protects Alcohol-Induced Hepatic Oxidative Stress but Worsens Liver Inflammation in Mice.Frontiers in pharmacology · 2021Article
- Neuronal Mitochondria Modulation of LPS-Induced Neuroinflammation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Pulmonary inflammation-induced alterations in key regulators of mitophagy and mitochondrial biogenesis in murine skeletal muscle.BMC pulmonary medicine · 2020Article
- Diesel Exhaust Particle Exposure Compromises Alveolar Macrophage Mitochondrial Bioenergetics.International journal of molecular sciences · 2019Article
- Differential placental ceramide levels during gestational diabetes mellitus (GDM).Reproductive biology and endocrinology : RB&E · 2019Article
- Impact of porcine reproductive and respiratory syndrome virus on muscle metabolism of growing pigs1.Journal of animal science · 2019Article
- Mitochondrial quality control mechanisms as potential therapeutic targets in sepsis-induced multiple organ failure.Journal of molecular medicine (Berlin, Germany) · 2019Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lipopolysaccharides (LPS) are prevalent pathogenic molecules that are found within tissues and blood. Elevated circulating LPS is a feature of obesity and sepsis, both of which are associated with mitochondrial abnormalities that are key pathological features of LPS excess. However, the mechanism of LPS-induced mitochondrial alterations remains poorly understood. Herein we demonstrate the necessity of sphingolipid accrual in mediating altered mitochondrial physiology in skeletal muscle following LPS exposure. In particular, we found LPS elicited disparate effects on the sphingolipids dihydroceramides (DhCer) and ceramides (Cer) in both cultured myotubes and in muscle of LPS-injected mice. Although LPS-treated myotubes had reduced DhCer and increased Cer as well as increased mitochondrial respiration, muscle from LPS-injected mice manifested a reverse trend, namely elevated DhCer, but reduced Cer as well as reduced mitochondrial respiration. In addition, we found that LPS treatment caused mitochondrial fission, likely via dynamin-related protein 1, and increased oxidative stress. However, inhibition of de novo sphingolipid biosynthesis via myriocin protected normal mitochondrial function in spite of LPS, but inhibition of DhCer desaturase 1, which increases DhCer, but not Cer, exacerbated mitochondrial respiration with LPS. In an attempt to reconcile the incongruent effects of LPS in isolated muscle cells and whole muscle tissue, we incubated myotubes with conditioned medium from treated macrophages. In contrast to direct myotube LPS treatment, conditioned medium from LPS-treated macrophages reduced myotube respiration, but this was again mitigated with sphingolipid inhibition. Thus, macrophage sphingolipid production appears to be necessary for LPS-induced mitochondrial alterations in skeletal muscle tissue.
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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.