ArticleExperimental biology and medicine (Maywood, N.J.)2021
MiR-296-5p ameliorates deep venous thrombosis by inactivating S100A4.
Article in Experimental biology and medicine (Maywood, N.J.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- The Role of Circulating MicroRNAs as Biomarkers and Therapeutic Targets in Venous Thromboembolism: A Systematic Review.Journal of clinical medicine · 2026Review
- The arterial-venous continuum: bridging atherosclerosis and chronic venous disease through endothelial dysfunction.Internal and emergency medicine · 2026Review
- MiR-582-3p regulates endothelial cell function in lower extremity deep vein thrombosis by targeting TFRC.Annals of hematology · 2026Article
- LncRNA MEG8 promotes deep vein thrombosis by sponging miR-296-5p to regulate human umbilical vein endothelial cells.Hereditas · 2025Article
- Identification of a key smooth muscle cell subset driving ischemic cardiomyopathy progression through single-cell RNA sequencing.Scientific reports · 2025Article
- Notoginsenoside Fc alleviates oxidized low-density lipoprotein-induced endothelial cell dysfunction and upregulates PPAR-γHistology and histopathology · 2024Article
- Diagnostic and prognostic potential of long non-coding RNA NORAD in patients with acute deep vein thrombosis and its role in endothelial cell function.Thrombosis journal · 2024Article
- Circulating miRNA profiles and the risk of hemorrhagic transformation after thrombolytic treatment of acute ischemic stroke: a pilot study.Frontiers in neurology · 2024Article
- MiRNAs and Their Role in Venous Thromboembolic Complications.Diagnostics (Basel, Switzerland) · 2023Review
- Depleted miR-125a-5p Causes Vascular Endothelial Cell Dysfunction in Deep Vein Thrombosis by Targeting Angiopoietin 2.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2023Article
- Suppression of long intergenic non-protein coding RNA 1123 constrains lower extremity deep vein thrombosis via microRNA-125a-3p to target interleukin 1 receptor type 1.Bioengineered · 2022Article
- LncRNA NEAT1 Promotes Vascular Endothelial Cell Dysfunction via miR-218-5p/GAB2 and Serves as a Diagnostic Biomarker for Deep Vein Thrombosis.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/HemostasisArticle
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12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deep venous thrombosis is one of the most common venous thromboembolic diseases and has a low cure rate and a high postoperative recurrence rate. Furthermore, emerging evidence indicates that microRNAs are involved in deep venous thrombosis. miR-296-5p is an important microRNA that plays a critical role in various cellular functions, and S100A4 is closely related to vascular function. miR-296-5p is downregulated in deep venous thrombosis patients, and its predicted target S100A4 is upregulated in deep venous thrombosis patients. Therefore, it was hypothesized that miR-296-5p may play a vital role in the development of deep venous thrombosis by targeting S100A4. An Ox-LDL-stimulated HUVEC and deep venous thrombosis mouse model was employed to detect the biological functions of miR-296-5p and S100A4. Dual luciferase reporter assays and pull-down assays were used to authenticate the interaction between miR-296-5p and S100A4. ELISA and Western blotting were employed to detect the protein levels of thrombosis-related factors and the endothelial-to-mesenchymal transition (EndMT)-related factors. The miR-296-5p levels were reduced, while the S100A4 levels were enhanced in deep venous thrombosis patients, and the miR-296-5p levels were negatively correlated with the S100A4 levels in deep venous thrombosis patients. miR-296-5p suppressed S100A4 expression by targeting the 3' UTR of S100A4. MiR-296-5p knockdown accelerated ox-LDL-induced HUVEC apoptosis, oxidative stress, thrombosis-related factor expression, and EndMT, while S100A4 knockdown antagonized these effects in ox-LDL-induced HUVECs. S100A4 knockdown reversed the effect induced by miR-296-5p knockdown. Moreover, the
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