ArticleMolecular medicine reports2019
Expression patterns of regulatory lncRNAs and miRNAs in muscular atrophy models induced by starvation in vitro and in vivo.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Epigenetics of Skeletal Muscle Atrophy.International journal of molecular sciences · 2024Review
- Combined analysis of lncRNA and mRNA emphasizes the potential role of tryptophan-mediated regulation of muscle development in weaned piglets by lncRNA.Journal of animal science · 2024Article
- Article
- Kampo formula hochu-ekki-to (Bu-Zhong-Yi-Qi-Tang, TJ-41) ameliorates muscle atrophy by modulating atrogenes and AMPK in vivo and in vitro.BMC complementary medicine and therapies · 2022Article
- Review
- TNF-α Induced Myotube Atrophy in C2C12 Cell Line Uncovers Putative Inflammatory-Related lncRNAs Mediating Muscle Wasting.International journal of molecular sciences · 2022Article
- Non-coding RNA basis of muscle atrophy.Molecular therapy. Nucleic acids · 2021Review
- Mitochondria and metabolic transitions in cardiomyocytes: lessons from development for stem cell-derived cardiomyocytes.Stem cell research & therapy · 2021Review
- Role of miRNAs and lncRNAs in dexamethasone-induced myotube atrophyExperimental and therapeutic medicine · 2021Article
- Regulation of Skeletal Muscle Atrophy in Cachexia by MicroRNAs and Long Non-coding RNAs.Frontiers in cell and developmental biology · 2020Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Starvation or severe deprivation of nutrients, which is commonly seen in surgical patients, can result in catabolic changes in skeletal muscles, such as muscle atrophy. Therefore, it is important to elucidate the underlying molecular regulatory mechanisms during skeletal muscle atrophy. In the present study, muscular atrophy was induced by starvation and the results demonstrated that myosin heavy chain was decreased, whereas muscle RING finger protein 1 and atrogin‑1 were increased, both in vitro and in vivo. The impact of starvation on the expression patterns of long non‑coding RNAs (lncRNAs) and microRNAs (miRNAs) was next determined. The expression patterns of miR‑23a, miR‑206 and miR‑27b in the starved mice exhibited similar trends as those in starved C2C12 cells in vitro, whereas the expression patterns of six other miRNAs (miR‑18a, miR‑133a, miR‑133b, miR‑186, miR‑1a and miR‑29b) differed between the in vivo and the in vitro starvation models. The present study indicated that in vitro expression of the selected miRNAs was not completely consistent with that in vivo. By contrast, lncRNAs showed excellent consistency in their expression patterns in both the in vitro and in vivo starvation models; six of the lncRNAs (Atrolnc‑1, long intergenic non‑protein coding RNA of muscle differentiation 1, Myolinc, lncRNA myogenic differentiation 1, Dum and muscle anabolic regulator 1) were significantly elevated in starved tissues and cells, while lnc‑mg was significantly decreased, compared with the control groups. Thus, lncRNAs involved in muscle atrophy have the potential to be developed as diagnostic tools.
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