ArticleCell communication and signaling : CCS2013
Phospholipase D regulates the size of skeletal muscle cells through the activation of mTOR signaling.
Article in Cell communication and signaling : CCS, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 36 citations in OpenAlex.
- Targeting FoxO1/3a, NF-κB, and mTOR signaling attenuates muscle atrophy in sepsis.Scientific reports · 2026Article
- Resistance exercise and skeletal muscle: protein synthesis, degradation, and controversies.European journal of applied physiology · 2025Review
- Skeletal muscle growth to combat diabetes and obesity: the potential role of muscle-secreted factors.Obesity (Silver Spring, Md.) · 2025Review
- Lin28a maintains a subset of adult muscle stem cells in an embryonic-like state.Cell research · 2023Article
- Activity-based directed evolution of a membrane editor in mammalian cells.Nature chemistry · 2023Article
- Whole-transcriptome analysis of rat cavernosum and identification of circRNA-miRNA-mRNA networks to investigate nerve injury erectile dysfunction pathogenesis.Bioengineered · 2021Article
- Transcriptome analysis reveals the long intergenic noncoding RNAs contributed to skeletal muscle differences between Yorkshire and Tibetan pig.Scientific reports · 2021Article
- Comparative Transcriptome and Methylome Analysis in Human Skeletal Muscle Anabolism, Hypertrophy and Epigenetic Memory.Scientific reports · 2019Article
- Phosphatidic acid: a lipid regulator of the Hippo pathway.Molecular & cellular oncology · 2019Article
- Regulation of the Hippo Pathway by Phosphatidic Acid-Mediated Lipid-Protein Interaction.Molecular cell · 2018Article
- Genes Whose Gain or Loss-Of-Function Increases Skeletal Muscle Mass in Mice: A Systematic Literature Review.Frontiers in physiology · 2018Article
- "Nutraceuticals" in relation to human skeletal muscle and exercise.American journal of physiology. Endocrinology and metabolism · 2017Review
- Phosphatidic acid: biosynthesis, pharmacokinetics, mechanisms of action and effect on strength and body composition in resistance-trained individuals.Nutrition & metabolism · 2017Review
- Kinetic disruption of lipid rafts is a mechanosensor for phospholipase D.Nature communications · 2016Article
- Mechanosensitive Molecular Networks Involved in Transducing Resistance Exercise-Signals into Muscle Protein Accretion.Frontiers in physiology · 2016Review
- Bone and skeletal muscle: Key players in mechanotransduction and potential overlapping mechanisms.Bone · 2015Review
- The phospholipase D superfamily as therapeutic targets.Trends in pharmacological sciences · 2015Review
- New strategy for in vitro activation of primordial follicles with mTOR and PI3K stimulators.Cell cycle (Georgetown, Tex.) · 2015Article
- Cellular and physiological roles for phospholipase D1 in cancer.The Journal of biological chemistry · 2014Review
- The role of diacylglycerol kinase ζ and phosphatidic acid in the mechanical activation of mammalian target of rapamycin (mTOR) signaling and skeletal muscle hypertrophy.The Journal of biological chemistry · 2014Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
mTOR is a major actor of skeletal muscle mass regulation in situations of atrophy or hypertrophy. It is established that Phospholipase D (PLD) activates mTOR signaling, through the binding of its product phosphatidic acid (PA) to mTOR protein. An influence of PLD on muscle cell size could thus be suspected. We explored the consequences of altered expression and activity of PLD isoforms in differentiated L6 myotubes. Inhibition or down-regulation of the PLD1 isoform markedly decreased myotube size and muscle specific protein content. Conversely, PLD1 overexpression induced muscle cell hypertrophy, both in vitro in myotubes and in vivo in mouse gastrocnemius. In the presence of atrophy-promoting dexamethasone, PLD1 overexpression or addition of exogenous PA protected myotubes against atrophy. Similarly, exogenous PA protected myotubes against TNFα-induced atrophy. Moreover, the modulation of PLD expression or activity in myotubes showed that PLD1 negatively regulates the expression of factors involved in muscle protein degradation, such as the E3-ubiquitin ligases Murf1 and Atrogin-1, and the Foxo3 transcription factor. Inhibition of mTOR by PP242 abolished the positive effects of PLD1 on myotubes, whereas modulating PLD influenced the phosphorylation of both S6K1 and Akt, which are respectively substrates of mTORC1 and mTORC2 complexes. These observations suggest that PLD1 acts through the activation of both mTORC1 and mTORC2 to induce positive trophic effects on muscle cells. This pathway may offer interesting therapeutic potentialities in the treatment of muscle wasting.
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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 Socratic graph.