ArticleInternational journal of molecular sciences2016
Atrogin-1 Deficiency Leads to Myopathy and Heart Failure in Zebrafish.
Article in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Atrogin-1 promotes muscle homeostasis by regulating levels of endoplasmic reticulum chaperone BiP.JCI insight · 2024Article
- Review
- Zebrafish Models for Skeletal Muscle Senescence: Lessons from Cell Cultures and Rodent Models.Molecules (Basel, Switzerland) · 2022Review
- CRISPR/Cas9-Mediated Constitutive Loss of VCP (Valosin-Containing Protein) Impairs Proteostasis and Leads to Defective Striated Muscle Structure and Function In Vivo.International journal of molecular sciences · 2022Article
- Histone deacetylase 1 controls cardiomyocyte proliferation during embryonic heart development and cardiac regeneration in zebrafish.PLoS genetics · 2021Article
- Gene alteration in zebrafish exposed to a mixture of substances of abuse.Environmental pollution (Barking, Essex : 1987) · 2021Article
- Exercise Training-IncreasedFrontiers in aging neuroscience · 2021Article
- Article
- Zebrafish Larvae Model of Dilated Cardiomyopathy Induced by Terfenadine.Korean circulation journal · 2017Article
- Studying Autophagy in Zebrafish.Cells · 2017Review
- Ftr82 Is Critical for Vascular Patterning during Zebrafish Development.International journal of molecular sciences · 2017Article
- Effects of Cobalt Chloride, a Hypoxia-Mimetic Agent, on Autophagy and Atrophy in Skeletal C2C12 Myotubes.BioMed research international · 2017Article
- "Muscling" Throughout Life: Integrating Studies of Muscle Development, Homeostasis, and Disease in Zebrafish.Current topics in developmental biology · 2017Review
- Cardiac ubiquitin ligases: Their role in cardiac metabolism, autophagy, cardioprotection and therapeutic potential.Biochimica et biophysica acta · 2016Review
- Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Orchestrated protein synthesis and degradation is fundamental for proper cell function. In muscle, impairment of proteostasis often leads to severe cellular defects finally interfering with contractile function. Here, we analyze for the first time the role of Atrogin-1, a muscle-specific E3 ubiquitin ligase known to be involved in the regulation of protein degradation via the ubiquitin proteasome and the autophagy/lysosome systems, in the in vivo model system zebrafish (Danio rerio). We found that targeted inactivation of zebrafish Atrogin-1 leads to progressive impairment of heart and skeletal muscle function and disruption of muscle structure without affecting early cardiogenesis and skeletal muscle development. Autophagy is severely impaired in Atrogin-1-deficient zebrafish embryos resulting in the disturbance of the cytoarchitecture of cardiomyocytes and skeletal muscle cells. These observations are consistent with molecular and ultrastructural findings in an Atrogin-1 knockout mouse and demonstrate that the zebrafish is a suitable vertebrate model to study the molecular mechanisms of Atrogin-1-mediated autophagic muscle pathologies and to screen for novel therapeutically active substances in high-throughput in vivo small compound screens (SCS).
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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.