ReviewJournal of neuromuscular diseases2016
"Get the Balance Right": Pathological Significance of Autophagy Perturbation in Neuromuscular Disorders.
Review in Journal of neuromuscular diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 47 citations in OpenAlex.
- Enhancement of Hypoxia-Induced Autophagy via the HIF-1apha/BNIP3 Pathway Promotes Proliferation and Myogenic Differentiation of Aged Skeletal Muscle Satellite Cells.Life (Basel, Switzerland) · 2026Article
- Obestatin Treatment Counteracts Muscle Wasting by Reactivation of Autophagy in Duchenne Muscular Dystrophy.MedComm · 2026Article
- Recent advances in the clinical spectrum and pathomechanisms associated with X-linked myopathy with excessive autophagy and otherJournal of neuromuscular diseases · 2025Review
- Changes to the Autophagy-Related Muscle Proteome Following Short-Term Treatment with Ectoine in the Duchenne Muscular Dystrophy Mouse Model mdx.International journal of molecular sciences · 2025Article
- TANGO2-related rhabdomyolysis symptoms are associated with abnormal autophagy functioning.Autophagy reports · 2024Article
- Changes in Physiopathological Markers in Myotonic Dystrophy Type 1 Skeletal Muscle: A 3-Year Follow-up Study.Journal of neuromuscular diseases · 2024Article
- Identification of a muscle-specific isoform of VMA21 as a potent actor in X-linked myopathy with excessive autophagy pathogenesis.Human molecular genetics · 2023Article
- A conserved STRIPAK complex is required for autophagy in muscle tissue.Molecular biology of the cell · 2023Article
- Activation of eIF4E-binding-protein-1 rescues mTORC1-induced sarcopenia by expanding lysosomal degradation capacity.Journal of cachexia, sarcopenia and muscle · 2023Article
- Gene Networks of Hyperglycemia, Diabetic Complications, and Human Proteins Targeted by SARS-CoV-2: What Is the Molecular Basis for Comorbidity?International journal of molecular sciences · 2022Article
- Silencing of the CaInternational journal of molecular sciences · 2022Article
- Cell interactome in sarcopenia during aging.Journal of cachexia, sarcopenia and muscle · 2022Article
- Autophagy in striated muscle diseases.Frontiers in cardiovascular medicine · 2022Review
- Common Pathogenic Mechanisms in Centronuclear and Myotubular Myopathies and Latest Treatment Advances.International journal of molecular sciences · 2021Review
- Autophagy in major human diseases.The EMBO journal · 2021Review
- Autophagy is affected in patients with hypokalemic periodic paralysis: an involvement in vacuolar myopathy?Acta neuropathologica communications · 2021Article
- The connection between the dynamic remodeling of the mitochondrial network and the regulation of muscle mass.Cellular and molecular life sciences : CMLS · 2021Review
- Defective lysosome reformation during autophagy causes skeletal muscle disease.The Journal of clinical investigation · 2021Article
- Indices of Defective Autophagy in Whole Muscle and Lysosome Enriched Fractions From Aged D2-mdx Mice.Frontiers in physiology · 2021Article
- Refining the Diagnosis of Growth-Related Muscle Abnormalities in Chickens Based on the Nomenclature Used to Characterise Human Myopathies.Frontiers in physiology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Recent research has revealed that autophagy, a major catabolic process in cells, is dysregulated in several neuromuscular diseases and contributes to the muscle wasting caused by non-muscle disorders (e.g. cancer cachexia) or during aging (i.e. sarcopenia). From there, the idea arose to interfere with autophagy or manipulate its regulatory signalling to help restore muscle homeostasis and attenuate disease progression. The major difficulty for the development of therapeutic strategies is to restore a balanced autophagic flux, due to the dynamic nature of autophagy. Thus, it is essential to better understand the mechanisms and identify the signalling pathways at play in the control of autophagy in skeletal muscle. A comprehensive analysis of the autophagic flux and of the causes of its dysregulation is required to assess the pathogenic role of autophagy in diseased muscle. Furthermore, it is essential that experiments distinguish between primary dysregulation of autophagy (prior to disease onset) and impairments as a consequence of the pathology. Of note, in most muscle disorders, autophagy perturbation is not caused by genetic modification of an autophagy-related protein, but rather through indirect alteration of regulatory signalling or lysosomal function. In this review, we will present the mechanisms involved in autophagy, and those ensuring its tight regulation in skeletal muscle. We will then discuss as to how autophagy dysregulation contributes to the pathogenesis of neuromuscular disorders and possible ways to interfere with this process to limit disease progression.
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.