ArticleJournal of cachexia, sarcopenia and muscle2022
The NLRP3 inflammasome contributes to inflammation-induced morphological and metabolic alterations in skeletal muscle.
Article in Journal of cachexia, sarcopenia and muscle, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07017517 (Effect of Physical Therapy on NLRP3 Inflammasome Activation and Muscle Atrophy in Critical Illness Myopathy), which is not on this map. Cited by 43 papers, 1 of them a synthesis that pooled it.
What it found
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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.
Effect of Physical Therapy on NLRP3 Inflammasome Activation and Muscle Atrophy in Critical Illness Myopathy (PT-NLRP3-CIM).
Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
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- Skeletal Muscle Fibre Type Determines Mitochondrial and Metabolic Responses to Hypoxia and Pulmonary Inflammation in Young Adult Rats.Journal of cachexia, sarcopenia and muscle · 2026Article
- The Role of Skeletal Muscle Mitochondria in NLRP3 Inflammasome Signaling.Biomolecules · 2026Review
- Muscle Dysfunction in Critical Illness: Established Mechanisms and the Potential Contribution of the NLRP3 Inflammasome.International journal of molecular sciences · 2026Review
- Statins promote muscle metabolic danger and NLRP3-mediated myopathy via lower protein-prenylation and YAP.Science advances · 2026Article
- Systemic Drivers and Molecular Mechanisms of Sarcopenia in Aetiology-Specific End-Stage Liver Disease.Journal of cachexia, sarcopenia and muscle · 2026Observational
- Skeletal Muscle Redox Signaling in Health and Disease: From Molecular Mechanisms to Therapeutic Exercise Strategies.Antioxidants (Basel, Switzerland) · 2026Review
- Systemic Inflammation Triggers Motor Axon Degeneration Via Macrophage IL-1β-Mediated P53/SIRT1/Autophagy Pathway.Inflammation · 2026Article
- Effects of Early Treatment with Lipid Core Nanoparticles-Associated Methotrexate on Cardiac Remodeling and Soleus Muscle Inflammasomes in Infarcted Rats.International journal of molecular sciences · 2026Article
- Sarcopenia and MASLD: novel insights and the future.Nature reviews. Endocrinology · 2026Review
- Article
- Hyaluronan 35 prevents endotoxin-mediated dysregulated skeletal muscle proteostasis during ethanol exposure.American journal of physiology. Endocrinology and metabolism · 2026Article
- The ageing microenvironment in sarcopenia: early alterations and targeted therapeutic strategies.Frontiers in immunology · 2026Review
- Targeting pyroptosis for skeletal muscle atrophy: mechanistic insights and therapeutic perspectives.Frontiers in immunology · 2026Review
- Cancer cachexia as an immunometabolic syndrome: targeting the immunometabolic interface with traditional Chinese Medicine monomers and formulas.Frontiers in immunology · 2026Review
- Integrative transcriptomic and experimental analyses prioritize TPT1 as a PANoptosis-associated candidate molecular marker in sarcopenia.Frontiers in cell and developmental biology · 2026Article
- Sarcopenia and sepsis fuel a self-perpetuating cycle of immunometabolism decline.Frontiers in immunology · 2026Review
- Sarcopenia in the Aging Process: Pathophysiological Mechanisms, Clinical Implications, and Emerging Therapeutic Approaches.International journal of molecular sciences · 2025Review
- RAGE contributes to persistent sepsis-induced muscle and mitochondrial alterations.Scientific reports · 2025Article
- Immune-mediated interactions between sarcopenia and atherosclerosis in aging.Immunity & ageing : I & A · 2025Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSystemic inflammation is associated with skeletal muscle atrophy and metabolic dysfunction. Although the nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome contributes to cytokine production in immune cells, its role in skeletal muscle is poorly understood. Here, we studied the link between inflammation, NLRP3, muscle morphology, and metabolism in in vitro cultured C2C12 myotubes, independent of immune cell involvement.
methodsDifferentiated C2C12 myotubes were treated with lipopolysaccharide (LPS; 0, 10, and 100-200 ng/mL) to induce activation of the NLRP3 inflammasome with and without MCC950, a pharmacological inhibitor of NLRP3-induced IL-1β production. We assessed markers of the NLRP3 inflammasome, cell diameter, reactive oxygen species, and mitochondrial function.
resultsNLRP3 gene expression and protein concentrations increased in a time-dependent and dose-dependent manner. Intracellular IL-1β concentration significantly increased (P < 0.0001), but significantly less with MCC950 (P = 0.03), suggestive of moderate activation of the NLRP3 inflammasome in cultured myotubes upon LPS stimulation. LPS suppressed myotube growth after 24 h (P = 0.03), and myotubes remained smaller up to 72 h (P = 0.0009). Exposure of myotubes to IL-1β caused similar alterations in cell morphology, and MCC950 mitigated these LPS-induced differences in cell diameter. NLRP3 appeared to co-localize with mitochondria, more so upon exposure to LPS. Mitochondrial reactive oxygen species were higher after LPS (P = 0.03), but not after addition of MCC950. Myotubes had higher glycolytic rates, and mitochondria were more fragmented upon LPS exposure, which was not altered by MCC950 supplementation.
conclusionsLPS-induced activation of the NLRP3 inflammasome in cultured myotubes contributes to morphological and metabolic alterations, likely due to its mitochondrial association.
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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.