ArticleScientific reports2023
Apelin is expressed in intimal smooth muscle cells and promotes their phenotypic transition.
Article in Scientific reports, 2023. 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, 8 citations in OpenAlex.
- Exercise-Induced Myokines in Obesity-Related Metabolic Disorders and Cardiovascular Protection: A Narrative Review.Sports (Basel, Switzerland) · 2026Review
- Age-related transcriptional drift and physiological adaptation in long-living Ames dwarf skeletal muscle.NAR molecular medicine · 2026Article
- S100A4 triggeres the pyroptosis of vsmcs: association with mitochondrial damage, impaired mitophagy, and CaBiology direct · 2026Article
- Association Between Apelin Gene -1860T>C (rs56204867) Polymorphism and Coronary Artery Disease in a Syrian Cohort.Vascular health and risk management · 2026Article
- The Impact of the Apelinergic System on the Cardiovascular System.International journal of molecular sciences · 2025Review
- CEMIP Maintains Vascular Contractility by Controlling PP1c-MLC20 Cascade in SMCs.Circulation research · 2025Article
- [Apelin promotes proliferation, migration, and angiogenesis in bladder cancer by activating the FGF2/FGFR1 pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- The "angiogenesis-plaque stability paradox" in atherosclerosis pathogenesis.Frontiers in cardiovascular medicine · 2025Review
- Liver B Cells Promotes MASLD Progression via the Apelin/APLNR System.International journal of medical sciences · 2025Article
- ACE2 deficiency inhibits thoracic aortic dissection by enhancing SIRT3 mediated inhibition of inflammation and VSCMs phenotypic switch.Molecular medicine (Cambridge, Mass.) · 2024Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During atherosclerotic plaque formation, smooth muscle cells (SMCs) switch from a contractile/differentiated to a synthetic/dedifferentiated phenotype. We previously isolated differentiated spindle-shaped (S) and dedifferentiated rhomboid (R) SMCs from porcine coronary artery. R-SMCs express S100A4, a calcium-binding protein. We investigated the role of apelin in this phenotypic conversion, as well as its relationship with S100A4. We found that apelin was highly expressed in R-SMCs compared with S-SMCs. We observed a nuclear expression of apelin in SMCs within experimentally-induced intimal thickening of the porcine coronary artery and rat aorta. Plasmids targeting apelin to the nucleus (N. Ap) and to the secretory vesicles (S. Ap) were transfected into S-SMCs where apelin was barely detectable. Both plasmids induced the SMC transition towards a R-phenotype. Overexpression of N. Ap, and to a lesser degree S. Ap, led to a nuclear localization of S100A4. Stimulation of S-SMCs with platelet-derived growth factor-BB, known to induce the transition toward the R-phenotype, yielded the direct interaction and nuclear expression of both apelin and S100A4. In conclusion, apelin induces a SMC phenotypic transition towards the synthetic phenotype. These results suggest that apelin acts via nuclear re-localization of S100A4, raising the possibility of a new pro-atherogenic relationship between apelin and S100A4.
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