ArticleMolecular therapy. Nucleic acids2020
Long Non-coding RNA PEBP1P2 Suppresses Proliferative VSMCs Phenotypic Switching and Proliferation in Atherosclerosis.
Article in Molecular therapy. Nucleic acids, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 62 citations in OpenAlex.
- Review
- PDK4 drives abdominal aortic aneurysm by promoting smooth muscle cell metabolic reprogramming and NLRP3-mediated pyroptosis.Nature communications · 2026Article
- The Role of Long Non-Coding RNA in Atherosclerosis: Mechanism and Intervention of Traditional Chinese Medicine.International journal of molecular sciences · 2026Review
- Circadian rhythms of gut microbiota and plaque vulnerability: mechanisms and chrono-microbiota modulation interventions.Gut microbes · 2025Review
- [Role of the TGFZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Review
- CircHAT1 regulates the proliferation and phenotype switch of vascular smooth muscle cells in lower extremity arteriosclerosis obliterans through targeting SFRS1.Molecular and cellular biochemistry · 2025Article
- Epigenetic regulation in coronary artery disease: from mechanisms to emerging therapies.Frontiers in molecular biosciences · 2025Review
- A Co-Culture System for Studying Cellular Interactions in Vascular Disease.Bioengineering (Basel, Switzerland) · 2024Review
- High glucose promotes atherosclerosis by regulating miRNA let7d-5p level.Journal of diabetes investigation · 2024Article
- CircTMEM165 facilitates endothelial repair by modulating mitochondrial fission via miR-192/SCP2iScience · 2024Article
- LncRNA CARMN inhibits abdominal aortic aneurysm formation and vascular smooth muscle cell phenotypic transformation by interacting with SRF.Cellular and molecular life sciences : CMLS · 2024Article
- Elucidating VSMC phenotypic transition mechanisms to bridge insights into cardiovascular disease implications.Frontiers in cardiovascular medicine · 2024Review
- Evidence Accumulates: Patients with Ascending Aneurysms Are Strongly Protected from Atherosclerotic Disease.International journal of molecular sciences · 2023Review
- Vascular smooth muscle cells enhance immune/vascular interplay in a 3-cell model of vascular inflammation.Scientific reports · 2023Article
- MicroRNA regulation of phenotypic transformations in vascular smooth muscle: relevance to vascular remodeling.Cellular and molecular life sciences : CMLS · 2023Review
- Insights into circular RNAs: Biogenesis, function and their regulatory roles in cardiovascular disease.Journal of cellular and molecular medicine · 2023Review
- Lnc_000048 Promotes Histone H3K4 Methylation of MAP2K2 to Reduce Plaque Stability by Recruiting KDM1A in Carotid Atherosclerosis.Molecular neurobiology · 2023Article
- Protective effect and mechanism of ginsenoside Rg2 on atherosclerosis.Journal of ginseng research · 2023Article
- Review
- Low expression of PEBP1P2 promotes metastasis of clear cell renal cell carcinoma by post-transcriptional regulation of PEBP1 and KLF13 mRNA.Experimental hematology & oncology · 2022Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non-coding RNAs (lncRNAs) play a crucial role in the growth of vascular smooth muscle cells (VSMCs), the dysfunction of which is closely associated with the initiation and progression of cardiovascular diseases (CVDs). Abnormal phenotypic switching and proliferation of VSMCs constitute a significant event in the progression of atherosclerosis. The present study identified a novel lncRNA, PEBP1P2, which serves as a valuable regulator of VSMCs in phenotypic transformation and proliferation. The expression of PEBP1P2 was remarkably decreased in proliferating VSMCs and pathological arteries when using a balloon injury model of rats. Furthermore, we found that PEBP1P2 represses proliferation, migration, and dedifferentiation during phenotype switching in VSMCs induced by platelet-derived growth factor BB (PDGF-BB). Mechanistically, cyclin-dependent kinase 9 (CDK9) was confirmed to be the direct target of PEBP1P2, which was proven to mediate phenotypic switching and proliferation of VSMCs and was rescued by PEBP1P2. Then, we explored the clinical significance, as we observed the decreased expression of PEBP1P2 in the serum of coronary heart disease (CHD) patients and human advanced carotid atherosclerotic plaques. Finally, PEBP1P2 overexpression distinctly suppressed neointima formation and VSMC phenotypic switching in vivo. Taken together, PEBP1P2 inhibits proliferation and migration in VSMCs by directly binding to CDK9, implying that it may be a promising therapeutic target for the treatment of proliferative vascular diseases.
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