miR-23 regulates cell proliferation and apoptosis of vascular smooth muscle cells in coronary heart disease
Open accessAbstract
BACKGROUND: Aberrant proliferation and migration of vascular smooth muscle cells (VSMCs) play an important role in the pathogenesis of cardiovascular diseases including coronary heart disease (CHD). MicroRNAs has reported play critical roles in VSMCs function. The present study was to investigate the effects of microRNA‑23 (miR-23) on VSMCs and uncover its potential mechanism. METHODS: Cell viability was detected by CCK-8 assay. Cell apoptosis was measured by flow cytometry. Dual luciferase reporter assay was conducted to verify whether BCL2L11 is a target gene of miR-23. The protein levels of BCL2L11 and caspase-3 were detect by quantitative real time PCR and western blot. RESULTS: Our results showed that the expression of miR-23 was upregulated in peripheral blood of CHD patients compared with controls. Overexpression of miR-23 promoted VSMCs proliferation and inhibited VSMCs apoptosis. Downregulation of miR-23 suppressed VSMCs proliferation and promoted VSMCs apoptosis. In addition, we identified BCL2L11 was a direct gene of miR-23. Overexpression of miR-23 decreased the levels of BCL2L11 and caspase-3, and downregulate of miR-23 increased the levels of BCL2L11and caspase-3 in VSMCs. CONCLUSION: Our findings suggest that miR-23 plays a crucial role in controlling VSMCs proliferation and apoptosis by targeting BCL2L11.
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miR-23 is upregulated in the peripheral blood of patients with coronary heart disease.
“Similarly, researchers have observed that miR-23 is also upregulated in the peripheral blood of patients with coronary heart disease (CHD).”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [49]
Overexpression of miR-23 can promote the proliferation of vascular smooth muscle cells and inhibit apoptosis through the target BCL2L11.
“Overexpression of miR-23 can promote the proliferation of VSMCs and inhibit apoptosis through another target BCL2L11 [49].”
From Recent advances of miR-23 in human diseases and growth development (2025) · cites this paper as [49]
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- Authors
- Liu, L., Cheng, Z., & Yang, J.
- Affiliations
- First Affiliated Hospital of Anhui Medical University (CN)
- Corresponding author
- Liu, Lijun
- ORCID
- Venue
- Pathology - Research and Practice
- Publisher
- Elsevier BV
- Published
- 2018-11
- Volume
- 214
- Issue
- 11
- Pages
- 1873-1878
- ISSN
- 0344-0338 (ISSN-L)
- OpenAlex
- W2889762767
- Cited by
- 28
- References
- 31
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 1 · 2023: 4 · 2022: 2 · 2021: 3 · 2020: 11 · 2019: 4
- FWCI
- 1.36
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Pathology - Research and Practice (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Keywords
- miR-23, microRNA, vascular smooth muscle cells, coronary artery disease, cell proliferation, apoptosis, BCL2L11, caspase-3, peripheral blood, miRNA target genes
- MeSH terms
- Bcl-2-Like Protein 11, Coronary Disease, Female, Gene Expression Regulation, Humans, Male, Muscle, Smooth, Vascular, Apoptosis, MicroRNAs, Cell Proliferation
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