ArticleDisease models & mechanisms2019
Article in Disease models & mechanisms, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 34 citations in OpenAlex.
- Article
- Editorial: Induced pluripotent stem cells (iPSCs) for skeletal muscle diseases.Frontiers in cell and developmental biology · 2025Article
- Aberrant evoked calcium signaling and nAChR cluster morphology in aFrontiers in cell and developmental biology · 2024Article
- Advancements in 2D and 3D In Vitro Models for Studying Neuromuscular Diseases.International journal of molecular sciences · 2023Review
- Caspase 3 exhibits a yeast metacaspase proteostasis function that protects mitochondria from toxic TDP43 aggregates.Microbial cell (Graz, Austria) · 2023Article
- Redox dysregulation as a driver for DNA damage and its relationship to neurodegenerative diseases.Translational neurodegeneration · 2023Review
- Patient-derived skin fibroblasts as a model to study frontotemporal lobar degeneration.Neural regeneration research · 2022Article
- The Cellular and Molecular Signature of ALS in Muscle.Journal of personalized medicine · 2022Review
- Dipeptide Repeat Pathology inAntioxidants (Basel, Switzerland) · 2022Article
- Metabolic Profile and Pathological Alterations in the Muscle of Patients with Early-Stage Amyotrophic Lateral Sclerosis.Biomedicines · 2022Article
- Mechanistic Insights of Mitochondrial Dysfunction in Amyotrophic Lateral Sclerosis: An Update on a Lasting Relationship.Metabolites · 2022Review
- Neuromuscular Junction Dysfunction in Amyotrophic Lateral Sclerosis.Molecular neurobiology · 2022Review
- Cell Surface Proteins for Enrichment andStem cells international · 2022Article
- Parkin beyond Parkinson's Disease-A Functional Meaning of Parkin Downregulation in TDP-43 Proteinopathies.Cells · 2021Review
- FTLD Patient-Derived Fibroblasts Show Defective Mitochondrial Function and Accumulation of p62.Molecular neurobiology · 2021Article
- Transcriptome analysis using patient iPSC-derived skeletal myocytes: Bet1L as a new molecule possibly linked to neuromuscular junction degeneration in ALS.Experimental neurology · 2021Article
- Evidence for the Role of Mitochondrial DNA Release in the Inflammatory Response in Neurological Disorders.International journal of molecular sciences · 2021Review
- Proteinopathies as Hallmarks of Impaired Gene Expression, Proteostasis and Mitochondrial Function in Amyotrophic Lateral Sclerosis.Frontiers in neuroscience · 2021Review
- Neuromuscular Development and Disease: Learning FromFrontiers in cell and developmental biology · 2021Review
- Age-dependent degeneration of an identified adult leg motor neuron in aBiology open · 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
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Amyotrophic lateral sclerosis (ALS) is a late-onset neuromuscular disease with no cure and limited treatment options. Patients experience a gradual paralysis leading to death from respiratory complications on average only 2-5 years after diagnosis. There is increasing evidence that skeletal muscle is affected early in the disease process, yet the pathological processes occurring in the skeletal muscle of ALS patients are still mostly unknown. Specifically, the most common genetic cause of ALS, a hexanucleotide repeat expansion in the
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.