ArticleInternational journal of molecular sciences2021
VEGFB Promotes Myoblasts Proliferation and Differentiation through VEGFR1-PI3K/Akt Signaling Pathway.
Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 53 citations in OpenAlex.
- miR-4687-3p modulates cell proliferation and migration in cervical cancer cells.Molecular biology reports · 2026Article
- Role of PI3K gene family as a molecular hub for regulation of growth and immunity: Potential implications for sustainable poultry production.Poultry science · 2026Review
- Aberrantly expressed long noncoding RNAs in adipose-derived mesenchymal stem cells differentiation to nucleus pulposus-like cells.Scientific reports · 2026Article
- RETRACTED: NFIC suppressed the development of Glioma via modulating the balance of SHP2/PI3K and NF-κB/PTEN Signaling.PloS one · 2026Article
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- Pro-Angiogenic Bioactive Molecules in Vascular Morphogenesis: Integrating Endothelial Cell Dynamics.Current issues in molecular biology · 2025Review
- Transcriptional Signatures of Aerobic Exercise-Induced Muscle Adaptations in Humans.Journal of functional morphology and kinesiology · 2025Article
- VEGF-B-mediated myofiber types involved in high-fat diet-induced hyperglycemia through PKA-NFATs signaling pathway.Stem cell research & therapy · 2025Article
- Mutual information stacking method for prediction of the growth traits in pigs.Briefings in bioinformatics · 2025Article
- Zearalenone Depresses Lactation Capacity Through the ROS-Mediated PI3K/AKT Pathway.Animals : an open access journal from MDPI · 2025Article
- Construction of the Red Swamp Crayfish (Genes · 2025Article
- The role of CLDN11 in promotion of granulosa cell proliferation in polycystic ovary syndrome via activation of the PI3K-AKT signalling pathway.Scientific reports · 2025Article
- Puerarin Promotes the Migration and Differentiation of Myoblasts by Activating the FAK and PI3K/AKT Signaling Pathways.Biology · 2025Article
- Multi-omics analysis of the biological function of the VEGF family in colon adenocarcinoma.Functional & integrative genomics · 2024Article
- Candidate circRNAs related to skeletal muscle development in Dazu black goats.Animal biotechnology · 2024Article
- Genome-scale CRISPR-Cas9 screen identifiesMedComm · 2024Article
- Article
- WIPF1 promotes gastric cancer progression by regulating PI3K/Akt signaling in a myocardin-dependent manner.iScience · 2023Article
- Vascular endothelial growth factor B improves impaired glucose tolerance through insulin-mediated inhibition of glucagon secretion.World journal of diabetes · 2023Article
- Role of m6A modification in regulating the PI3K/AKT signaling pathway in cancer.Journal of translational medicine · 2023Review
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Authors and funding
16 authors at 1 institution in 1 country.
Funding
Abstract
It has been demonstrated that vascular endothelial growth factor B (VEGFB) plays a vital role in regulating vascular biological function. However, the role of VEGFB in regulating skeletal muscle cell proliferation and differentiation remains unclear. Thus, this study aimed to investigate the effects of VEGFB on C2C12 myoblast proliferation and differentiation and to explore the underlying mechanism. For proliferation, VEGFB significantly promoted the proliferation of C2C12 myoblasts with the upregulating expression of cyclin D1 and PCNA. Meanwhile, VEGFB enhanced vascular endothelial growth factor receptor 1 (VEGFR1) expression and activated the PI3K/Akt signaling pathway in a VEGFR1-dependent manner. In addition, the knockdown of VEGFR1 and inhibition of PI3K/Akt totally abolished the promotion of C2C12 proliferation induced by VEGFB, suggesting that VEGFB promoted C2C12 myoblast proliferation through the VEGFR1-PI3K/Akt signaling pathway. Regarding differentiation, VEGFB significantly stimulated the differentiation of C2C12 myoblasts via VEGFR, with elevated expressions of MyoG and MyHC. Furthermore, the knockdown of VEGFR1 rather than NRP1 eliminated the VEGFB-stimulated C2C12 differentiation. Moreover, VEGFB activated the PI3K/Akt/mTOR signaling pathway in a VEGFR1-dependent manner. However, the inhibition of PI3K/Akt/mTOR blocked the promotion of C2C12 myoblasts differentiation induced by VEGFB, indicating the involvement of the PI3K/Akt pathway. To conclude, these findings showed that VEGFB promoted C2C12 myoblast proliferation and differentiation via the VEGFR1-PI3K/Akt signaling pathway, providing new insights into the regulation of skeletal muscle development.
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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.