ArticleInternational urology and nephrology2022
MiR-133a is a potential target for arterial calcification in patients with end-stage renal disease.
Article in International urology and nephrology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.
- The characteristic expression of circulatingFrontiers in endocrinology · 2024Pooled it
- Review
- Association of miR-133a With Microalbuminuria in Patients With Resistant Arterial Hypertension and Chronic Kidney Disease.Medical science monitor : international medical journal of experimental and clinical research · 2026Article
- Review
- Advances in the study of miRNAs in chronic kidney disease with cardiovascular complications.Frontiers in physiology · 2023Review
- MicroRNAs and vascular damage in chronic kidney disease: advances and clinical implications.Jornal brasileiro de nefrologiaReview
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundArterial calcification is an important risk factor for patients with end-stage renal disease. Despite substantial research efforts, the detailed mechanisms of the process of arterial calcification in end-stage renal disease remain unclear.
methodsmiR-133a expression in radial artery samples was detected by FISH and Alizarin Red Staining. The expressions of miR-133a and RUNX2 in A7r5 cells with BMP2 induction were detected by qRT-PCR. In addition, qRT-PCR, Western blot, and ELISA assay were performed to detect changes in miR-133a levels in A7R5 cells after different treatments.
resultsAlizarin Red staining showed that red crystal deposition occurred in the tunica media. FISH analysis indicated that miR-133a was upregulated in the tunica media of the radial artery samples without calcification when compared with those with calcification. We also found that expression of RUNX2 in A7r5 cells increased at day 7 and day 14 after BMP2 induction and decreased miR-133a expression decreased at day 14. In addition, RUNX2 protein and OCN expression were upregulated in A7r5 cells during BMP2-induced calcification. When miR-133a expression was suppressed, cell calcification aggravated, which led to upregulation of RUNX2 and OCN. When miR-133a was overexpressed, calcification of cells was inhibited, resulting in downregulation of RUNX2 and OCN.
conclusionThe present study reveals that miR-133a could indirectly regulate cell calcification through the RUNX2 gene expression. Our findings provide insight into the potential use of miR-133a as a molecular target for diagnosing vascular calcification in end-stage renal disease.
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