ReviewFrontiers in neuroscience2015
The unfolded protein response in multiple sclerosis.
Review in Frontiers in neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 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
66 citing papers in PubMed, 102 citations in OpenAlex.
- Tmem117, an oligodendrocyte-enriched regulator of NCX activity, links myelin homeostasis to counterregulation and metabolic health.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Characterizing the impact of plasma protein levels on human brain structure and disorders leveraging integrative multi-omics analysis.medRxiv : the preprint server for health sciences · 2026Article
- Proteomic Profiling of Optic Nerves From SMOX-Deficient Mice Identifies Regulators of Neuroinflammation and Axonal Damage in Optic Neuritis.Investigative ophthalmology & visual science · 2026Article
- Emerging perspectives in proteostasis: bridging mechanisms and therapeutics for human diseases.Signal transduction and targeted therapy · 2026Review
- Neuromodulatory role and therapeutic potential of N 6 -methyladenosine RNA methylation in neurodegenerative diseases.Neural regeneration research · 2026Article
- A comparative transcriptomic analysis of mouse demyelination models and multiple sclerosis lesions.Nature communications · 2026Article
- Senolytic treatment induces oligodendrocyte dysfunction and demyelination in the corpus callosum.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Glial Cell Dynamics in Neuroinflammation: Mechanisms, Interactions, and Therapeutic Implications.Biomedicines · 2026Review
- Review
- The interplay between endoplasmic reticulum stress and inflammation in multiple sclerosis.Scientific reports · 2025Article
- Neuroprotective strategies in multiple sclerosis: a status update and emerging paradigms.Expert review of neurotherapeutics · 2025Review
- AA147 Alleviates Symptoms in a Mouse Model of Multiple Sclerosis by Reducing Oligodendrocyte Loss.Glia · 2025Article
- Broad rim lesions are a new pathological and imaging biomarker for rapid disease progression in multiple sclerosis.Nature medicine · 2025Article
- Exploring the Causal Association Between 91 Circulating Inflammatory Proteins and Neurodegenerative Diseases: A Bidirectional Two-Sample Mendelian Randomization and Bioinformatics Analysis.Brain and behavior · 2025Article
- Thinning of originally-existing, mature myelin represents a nondestructive form of myelin loss in the adult CNS.Frontiers in cellular neuroscience · 2025Article
- Endoplasmic reticulum's role in multiple sclerosis, exploring potential biomarkers, and pioneering therapeutic strategies: a comprehensive review of literature.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Review
- Machine Learning Analysis Using RNA Sequencing to Distinguish Neuromyelitis Optica from Multiple Sclerosis and Identify Therapeutic Candidates.The Journal of molecular diagnostics : JMD · 2024Article
- Automated analysis of gray matter damage in aged mice reveals impaired remyelination in the cuprizone model.Brain pathology (Zurich, Switzerland) · 2024Article
- Review
- Mechanisms Governing Oligodendrocyte Viability in Multiple Sclerosis and Its Animal Models.Cells · 2024Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The unfolded protein response (UPR) occurs in response to endoplasmic reticulum (ER) stress caused by the accumulation of unfolded or misfolded proteins in the ER. The UPR is comprised of three signaling pathways that promote cytoprotective functions to correct ER stress; however, if ER stress cannot be resolved the UPR results in apoptosis of affected cells. The UPR is an important feature of various human diseases, including multiple sclerosis (MS). Recent studies have shown several components of the UPR are upregulated in the multiple cell types in MS lesions, including oligodendrocytes, T cells, microglia/macrophages, and astrocytes. Data from animal model studies, particularly studies of experimental autoimmune encephalomyelitis (EAE) and the cuprizone model, imply an important role of the UPR activation in oligodendrocytes in the development of MS. In this review we will cover current literature on the UPR and the evidence for its role in the development of MS.
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.