ArticleCell biology international2019
Oxidized low-density lipoprotein promotes vascular endothelial cell dysfunction by stimulating miR-496 expression and inhibiting the Hippo pathway effector YAP.
Article in Cell biology international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Neointimal hyperplasia and vascular restenosis: from molecular mechanisms to therapeutic interventions.Molecular biomedicine · 2026Review
- Differential microRNA profiling of the Marshallese population in Arkansas reveals a higher association with chronic diseases.PloS one · 2025Article
- YAP/TAZ as mechanobiological signaling pathway in cardiovascular physiological regulation and pathogenesis.Mechanobiology in medicine · 2024Article
- Identification of plasma miR-4505, miR-4743-5p and miR-4750-3p as novel diagnostic biomarkers for coronary artery disease in patients with type 2 diabetes mellitus: a case-control study.Cardiovascular diabetology · 2024Article
- Molecular Morbidity Score-Can MicroRNAs Assess the Burden of Disease?International journal of molecular sciences · 2024Review
- Vascular endothelial cellular mechanics under hyperglycemia and its role in tissue regeneration.Regenerative biomaterials · 2024Article
- Non-coding RNAs as regulators of the Hippo pathway in cardiac development and cardiovascular disease.Frontiers in pharmacology · 2024Review
- Decreased expression ofAmerican journal of clinical and experimental urology · 2024Article
- The Potential Role of Connexins in the Pathogenesis of Atherosclerosis.International journal of molecular sciences · 2023Review
- Yes-Associated Protein and Transcriptional Coactivator with PDZ-Binding Motif in Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- Distinctive Roles of YAP and TAZ in Human Endothelial Progenitor Cells Growth and Functions.Biomedicines · 2022Article
- The Association Between Hyperlipidemia and In-Hospital Outcomes in Takotsubo Cardiomyopathy.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Article
- Yes-Associated Protein in Atherosclerosis and Related Complications: A Potential Therapeutic Target That Requires Further Exploration.Frontiers in cardiovascular medicine · 2021Review
- MicroRNA-496 suppresses tumor cell proliferation by targeting BDNF in osteosarcoma.Experimental and therapeutic medicine · 2020Article
- Angiotensin type 1 receptor regulates yes-associated protein in vascular endothelial cells.Experimental and therapeutic medicine · 2020Article
- The Circular RNA circRNA124534 Promotes Osteogenic Differentiation of Human Dental Pulp Stem Cells Through Modulation of the miR-496/β-Catenin Pathway.Frontiers in cell and developmental biology · 2020Article
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Oxidized low-density lipoprotein (ox-LDL) can damage vascular endothelial cells and cause atherosclerosis, but its epigenetic regulatory mechanism has not been fully elucidated. We show that ox-LDL induced significant apoptosis and loss of function in human umbilical vascular endothelial cells (HUVECs). At the same time, ox-LDL significantly decreased the expression of Hippo-YAP/ZAP (Yes-associated protein/YLP motif-containing 1) pathway proteins as compared to that of the control. The luciferase reporter system confirmed that microRNA (miR)-496 silenced YAP gene expression by binding to its 3' untranslated region (3' UTR). Ox-LDL-treated miR-496 overexpression HUVECs had a higher apoptosis rate and more severe dysfunction compared to the control cells. This in-depth study shows that ox-LDL inhibits YAP protein expression by inducing miR-496 expression, leading to its inability to enter the nucleus, thereby losing its function as a transcriptional cofactor for activating the downstream genes. Our findings reveal that, through epigenetic modification, ox-LDL can inhibit the normal expression of Hippo-YAP/ZAP pathway proteins via miR-496 expression and induce vascular endothelial cell dysfunction.
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