ArticlePloS one2015
Antioxidant Treatment and Induction of Autophagy Cooperate to Reduce Desmin Aggregation in a Cellular Model of Desminopathy.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 31 citations in OpenAlex.
- BAG3 gene therapy emerges as a potential treatment for myofibrillar myopathies.Molecular therapy. Advances · 2026Article
- Intermediate filaments and their associated molecules.Journal of biomedical research · 2025Article
- Potential Vitamin E Signaling Mediators in Skeletal Muscle.Antioxidants (Basel, Switzerland) · 2024Review
- Desmin Reorganization by Stimuli Inducing Oxidative Stress and Electrophiles: Role of Its Single Cysteine Residue.Antioxidants (Basel, Switzerland) · 2023Article
- Dominant-negative p53-overexpression in skeletal muscle induces cell death and fiber atrophy in rats.Cell death & disease · 2022Article
- Desmin variants: Trigger for cardiac arrhythmias?Frontiers in cell and developmental biology · 2022Review
- Skeletal and Cardiac Muscle Disorders Caused by Mutations in Genes Encoding Intermediate Filament Proteins.International journal of molecular sciences · 2021Review
- A cytoplasmic escapee: desmin is going nuclear.Turkish journal of biology = Turk biyoloji dergisi · 2021Review
- Generation of desminopathy in rats using CRISPR-Cas9.Journal of cachexia, sarcopenia and muscle · 2020Article
- Article
- Targeting and extending the eukaryotic druggable genome with natural products: cytoskeletal targets of natural products.Natural product reports · 2020Review
- Come Together: Protein Assemblies, Aggregates and the Sarcostat at the Heart of Cardiac Myocyte Homeostasis.Frontiers in physiology · 2020Review
- The Autophagy Signaling Pathway: A Potential Multifunctional Therapeutic Target of Curcumin in Neurological and Neuromuscular Diseases.Nutrients · 2019Review
- Proteome and transcriptome profiling of equine myofibrillar myopathy identifies diminished peroxiredoxin 6 and altered cysteine metabolic pathways.Physiological genomics · 2018Article
- Molecular insights into cardiomyopathies associated with desmin (DES) mutations.Biophysical reviews · 2018Review
- The role of αB-crystallin in skeletal and cardiac muscle tissues.Cell stress & chaperones · 2018Review
- Redox Control of Skeletal Muscle Regeneration.Antioxidants & redox signaling · 2017Review
- Sevoflurane Ameliorates Myocardial Cell Injury by Inducing Autophagy via the Deacetylation of LC3 by SIRT1.Analytical cellular pathology (Amsterdam) · 2017Article
- Myofibrillar Myopathies: New Perspectives from Animal Models to Potential Therapeutic Approaches.Journal of neuromuscular diseases · 2017Review
- Disrupted autophagy undermines skeletal muscle adaptation and integrity.Mammalian genome : official journal of the International Mammalian Genome Society · 2016Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Desminopathies, a subgroup of myofibrillar myopathies (MFMs), the progressive muscular diseases characterized by the accumulation of granulofilamentous desmin-positive aggregates, result from mutations in the desmin gene (DES), encoding a muscle-specific intermediate filament. Desminopathies often lead to severe disability and premature death from cardiac and/or respiratory failure; no specific treatment is currently available. To identify drug-targetable pathophysiological pathways, we performed pharmacological studies in C2C12 myoblastic cells expressing mutant DES. We found that inhibition of the Rac1 pathway (a G protein signaling pathway involved in diverse cellular processes), antioxidant treatment, and stimulation of macroautophagy reduced protein aggregation by up to 75% in this model. Further, a combination of two or three of these treatments was more effective than any of them alone. These results pave the way towards the development of the first treatments for desminopathies and are potentially applicable to other muscle or brain diseases associated with abnormal protein aggregation.
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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.