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MiR-582-3p regulates endothelial cell function in lower extremity deep vein thrombosis by targeting TFRC
Qiulian Luo1, Anni Xu2, Min Liang3
1Department of Hematology, Yiwu Central Hospital, Yiwu, 322000, China.
Annals of Hematology
|May 20, 2026
Summary
MicroRNA-582-3p is downregulated in lower extremity deep vein thrombosis (LEDVT) and acts as a protective factor. This microRNA targets TFRC, offering potential as a diagnostic biomarker and therapeutic target for LEDVT.
Area of Science:
- Molecular Biology
- Biochemistry
- Vascular Biology
Background:
- MicroRNAs (miRNAs) are crucial in regulating gene expression and have been implicated in various diseases, including deep vein thrombosis.
- The specific role and mechanism of miR-582-3p in lower extremity deep vein thrombosis (LEDVT) remain largely unexplored.
- Understanding miRNA involvement is key to developing novel diagnostic and therapeutic strategies for LEDVT.
Purpose of the Study:
- To investigate the expression levels of miR-582-3p in patients with LEDVT and in a human umbilical vein endothelial cell (HUVEC) model.
- To elucidate the regulatory function and molecular mechanism of miR-582-3p in LEDVT pathogenesis.
- To assess the diagnostic potential and protective role of miR-582-3p in LEDVT.
Main Methods:
- Quantitative reverse transcription polymerase chain reaction (RT-qPCR) to measure miR-582-3p and TFRC expression.
- Construction of an ox-LDL-induced HUVEC injury model to mimic LEDVT conditions.
- Cellular assays (CCK8, flow cytometry, ELISA) to evaluate cell proliferation, apoptosis, and inflammatory responses.
- Dual-luciferase reporter assays and rescue experiments to confirm the targeting relationship between miR-582-3p and TFRC.
Main Results:
- MiR-582-3p was significantly downregulated in LEDVT patients' serum and ox-LDL-treated HUVECs, correlating negatively with D-dimer and TAT III levels.
- MiR-582-3p demonstrated a high diagnostic value (AUC=0.870) and acted as an independent protective factor against LEDVT.
- Overexpression of miR-582-3p promoted HUVEC proliferation, inhibited apoptosis, reduced inflammatory factors (TNF-α, IL-1β, IL-6), and modulated coagulation factors.
- MiR-582-3p directly targeted TFRC, and TFRC overexpression counteracted the protective effects of miR-582-3p in ox-LDL-induced HUVEC damage.
Conclusions:
- MiR-582-3p is a potential diagnostic biomarker and an independent protective factor for LEDVT.
- MiR-582-3p regulates endothelial cell function and inflammatory responses by targeting TFRC.
- MiR-582-3p represents a promising therapeutic target for managing LEDVT.
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