ArticleClinical and translational science2014
Cytokine profiling in patients with VCP-associated disease.
Article in Clinical and translational science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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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.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
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- Article
- Secretome from Uterine Cervical Mesenchymal Stem Cells as a Protector of Neuronal Cells Against Oxidative Stress and Inflammation.Biomolecules · 2025Article
- VCP Inhibition Augments NLRP3 Inflammasome Activation.Inflammation · 2024Article
- Clinical Classification of Variants in the Valosin-Containing Protein Gene Associated With Multisystem Proteinopathy.Neurology. Genetics · 2023Article
- Valosin-containing protein (VCP/p97) inhibition reduces viral clearance and induces toxicity associated with muscular damage.Cell death & disease · 2022Article
- Remifentanil inhibits the inflammatory response of BV2 microglia and protects PC12 cells from damage caused by microglia activation.Bioengineered · 2022Article
- Valosin-containing protein-regulated endoplasmic reticulum stress causes NOD2-dependent inflammatory responses.Scientific reports · 2022Article
- TDP-43 and Inflammation: Implications for Amyotrophic Lateral Sclerosis and Frontotemporal Dementia.International journal of molecular sciences · 2021Review
- Cyanidin-3-O-Glucoside Protects PC12 Cells Against Neuronal Apoptosis Mediated by LPS-Stimulated BV2 Microglial Activation.Neurotoxicity research · 2020Article
- Neuroinflammation in frontotemporal dementia.Nature reviews. Neurology · 2019Review
- Activation of the NLRP3 Inflammasome Is Associated with Valosin-Containing Protein Myopathy.Inflammation · 2017Article
- Protocatechuic Acid Inhibits Inflammatory Responses in LPS-Stimulated BV2 Microglia via NF-κB and MAPKs Signaling Pathways.Neurochemical research · 2015Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
Valosin containing protein (VCP) disease (also known as Inclusion Body Myopathy, Paget Disease of Bone and Frontotemporal Dementia [IBMPFD] syndrome) is caused by mutations in the gene encoding VCP classically affecting the muscle, bone and brain. Although the genetic cause has been identified, details regarding the pathogenesis of IBMPFD have not been fully determined. Muscle wasting observed in VCP disease is suggestive of cytokine imbalance. We hypothesized that dysfunctional protein homeostasis caused by VCP mutations leads to cytokine imbalances thereby contributing to the muscle wasting phenotype. Circulating levels of interleukin-4 (IL-4), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF a) and epidermal growth factor (EGF) were measured in plasma of patients with VCP disease or controls. TNF a and EGF were significantly altered in VCP disease as compared to control. TNF a was up-regulated, consistent with a cachexia phenotype and EGF levels were increased. No significant differences were observed in IL-4 and IL-6. Cytokine imbalances may be associated with VCP disease and may play a contributory role in VCP myopathy. Further understanding of how VCP dysfunction leads to aberrant protein homeostasis and subsequent cytokine imbalances may also aid in the understanding of other proteinopathies and in the development of novel treatments.
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Registered trials
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