ArticleJournal of cachexia, sarcopenia and muscle2018
The double-edged sword of endoplasmic reticulum stress in uremic sarcopenia through myogenesis perturbation.
Article in Journal of cachexia, sarcopenia and muscle, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
- Understanding the gut microbiota and sarcopenia: a systematic review.Journal of cachexia, sarcopenia and muscle · 2021Pooled it
- Chronic Kidney Disease, Sarcopenia, and Hormonal-Metabolic Alterations: An Intriguing Association.Kidney & blood pressure research · 2026Review
- Effect of fermented soy protein isolates containing collagen (Soylagen) on muscle atrophy: insight from network pharmacology analysis and experimental evidence.Frontiers in pharmacology · 2026Article
- Predictive utility of nomogram based on serum glucose-regulated protein 78 and kidney function for long-term kidney graft survival.Scientific reports · 2024Article
- Pathogenesis of Sarcopenia in Chronic Kidney Disease-The Role of Inflammation, Metabolic Dysregulation, Gut Dysbiosis, and microRNA.International journal of molecular sciences · 2024Review
- Association of endothelial dysfunction and peripheral arterial disease with sarcopenia in chronic kidney disease.Journal of cachexia, sarcopenia and muscle · 2024Article
- Insights into the underlying pathogenesis and therapeutic potential of endoplasmic reticulum stress in degenerative musculoskeletal diseases.Military Medical Research · 2023Review
- Endoplasmic reticulum stress: a novel targeted approach to repair bone defects by regulating osteogenesis and angiogenesis.Journal of translational medicine · 2023Review
- Emodin Inhibits the Indoxyl Sulfate-Induced trans-Differentiation of Vascular Smooth Muscle Cells through Upregulating Thrombospondin-1.Journal of vascular research · 2023Article
- Indoxyl sulfate mediates low handgrip strength and is predictive of high hospitalization rates in patients with end-stage renal disease.Frontiers in medicine · 2023Article
- Selenoprotein K protects skeletal muscle from damage and is required for satellite cells-mediated myogenic differentiation.Redox biology · 2022Article
- Ryanodine receptor RyR1-mediated elevation of CaJournal of animal science and biotechnology · 2022Article
- Article
- Review
- Uremic Toxins and Frailty in Patients with Chronic Kidney Disease: A Molecular Insight.International journal of molecular sciences · 2021Review
- β2-adrenergic receptor agonist counteracts skeletal muscle atrophy and oxidative stress in uremic mice.Scientific reports · 2021Article
- Uraemic toxins impair skeletal muscle regeneration by inhibiting myoblast proliferation, reducing myogenic differentiation, and promoting muscular fibrosis.Scientific reports · 2021Article
- Review
- MicroRNA-mRNA Co-sequencing Identifies Transcriptional and Post-transcriptional Regulatory Networks Underlying Muscle Wasting in Cancer Cachexia.Frontiers in genetics · 2020Article
- Berberine Down-Regulated Myostatin Expression and Facilitated Metabolism via Smad Pathway in Insulin Resistant Mice.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSarcopenia is the age-related degeneration characterized with the decline of skeletal muscle mass, strength, and function. The imbalance of protein synthesis and degradation which jeopardizes immune, hormone regulation, and muscle-motor neuron connection is the main cause of sarcopenia. There is limited knowledge regarding molecular mechanism of sarcopenia. As the endoplasmic reticulum is the control centre of the protein syntheses and degradation, we hypothesized that endoplasmic reticulum stress and unfolded protein response (UPR) play an important in the development of sarcopenia. Understanding the sarcopenia molecular mechanisms may benefit the therapeutic diagnosis and treatment in the future.
methodsMouse myoblast C2C12 cells are exposed to designated time and concentration of indoxyl sulfate (IS), a uremic toxin of chronic kidney disease. The proliferation, differentiation, and the expression of atrogin 1 are examined. The protein and mRNA expression of IS treated-C2C12 cells are inspected to distinguish the role of ER stress and oxidative stress underlying the sarcopenia.
resultsIndoxyl sulfate inhibits myoblast differentiation. We demonstrate that as the number of multi-nuclei myotube decreased, the differentiation markers including myoD, myoG, and myosin heavy chain are also suppressed. Indoxyl sulfate inhibits myoblast proliferation and induces the myotubular atrophy marker atrogin-1 protein expression. Indoxyl sulfate stimulates eIF2α phosphorylation and XBP1 mRNA splicing in UPR. Interestingly, the oxidative stress is related to eIF2α phosphorylation but not XBP1 mRNA splicing. The eIF2α phosphorylation triggered by IS reduces myoD, myoG, and myosin heavy chain protein expression, which represents the anti-myogenic modulation on the early differentiation event. The XBP1 mRNA splicing induced by IS, however, is considered the adaptive response to restore the myogenic differentiation.
conclusionsOur studies indicated that the ER stress and UPR modulation are critical in the chronic kidney disease uremic toxin-accumulated sarcopenia model. We believe that UPR-related signals showed great potential in clinical application.
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.