ArticleMolecular and cellular biochemistry2020
MALAT1 affects hypoxia-induced vascular endothelial cell injury and autophagy by regulating miR-19b-3p/HIF-1α axis.
Article in Molecular and cellular biochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 51 citations in OpenAlex.
- Review
- Article
- Long non-coding RNA LINC00607 epigenetically regulates endothelial TSPAN18 to promote hypoxia-induced thromboinflammation.The Journal of biological chemistry · 2026Article
- Construction and Analysis of Immune Infiltration and Competing Endogenous RNA Network in Moyamoya Disease.International journal of molecular sciences · 2025Article
- The roles of lncMALAT1 in coronary artery disease regulation and therapeutic perspective: A systematic review.iScience · 2025Article
- Macrophage-derived lncRNAs in cancer: regulators of tumor progression and therapeutic targets.Medical oncology (Northwood, London, England) · 2025Review
- A miRNA cocktail orchestrates coordinated cellular responses to promote diabetic wound healing.Burns & trauma · 2025Article
- Cardiovascular diseases in the elderly: possibilities for modulating autophagy using non-coding RNAs.Frontiers in cell and developmental biology · 2025Review
- The Diagnosis and Prognosis Value of Circulating Exosomal lncRNA MALAT1 and LNC_000226 in Patients With Acute Myocardial Infarction: An Observational Study.Immunity, inflammation and disease · 2024Observational
- LncRNAs Are Key Regulators of Transcription Factor-Mediated Endothelial Stress Responses.International journal of molecular sciences · 2024Review
- Induction of lncRNA MALAT1 by hypoxia promotes bone formation by regulating the miR-22-3p/CEBPD axis.Histology and histopathology · 2023Article
- Establishing a prediction model of severe acute mountain sickness using machine learning of support vector machine recursive feature elimination.Scientific reports · 2023Article
- Extracellular vesicles in atherosclerosis and vascular calcification: the versatile non-coding RNAs from endothelial cells and vascular smooth muscle cells.Frontiers in medicine · 2023Review
- MiR-29b-3p Inhibits the Inflammation Injury in Human Umbilical Vein Endothelial Cells by Regulating SEC23A.Biochemical genetics · 2022Article
- Review
- Exploring the role of non-coding RNAs in autophagy.Autophagy · 2022Review
- Regulatory Non-coding RNAs in Atherosclerosis.Handbook of experimental pharmacology · 2022Review
- Identification of MicroRNA-Potassium Channel Messenger RNA Interactions in the Brain of Rats With Post-traumatic Epilepsy.Frontiers in molecular neuroscience · 2020Article
- Ketamine ameliorates hypoxia-induced endothelial injury in human umbilical vein endothelial cells.Clinics (Sao Paulo, Brazil) · 2020Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiovascular disease has become the leading cause of death in the world. Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) plays an important role in cardiovascular disease, such as stroke. However, the role of MALAT1 in hypoxia (HYP)-induced vascular endothelial cells (VECs) remains unclear. In the present study, HYP-treated human umbilical vein endothelial cells (HUVECs) were utilized to simulate HYP-induced VEC injury. It was found that after HYP treatment, the levels of MALAT1 and hypoxia-induced factor-1 (HIF-1α) in HUVECs were upregulated, while the level of miR-19b-3p was downregulated. Knockdown of MALAT1 with siRNA significantly reduced the HIF-1α level induced by HYP. In addition, MALAT1 knockdown inhibited HYP-induced HUVECs apoptosis, autophagy and inflammation. The overexpression of HIF-1α overcame the effect of MALAT1 knockdown. Mechanism analysis showed that MALAT1-targeted miR-19b-3p and then regulated downstream HIF-1α. MALAT1 knockdown increased the level of miR-19b-3p in cells, and increased miR-19b-3p further inhibited the expression of HIF-1α, thereby reducing the HYP-induced HUVECs apoptosis, autophagy and inflammation. Taken together, these results suggest that MALAT1 may be a potential target for mitigating HYP-induced endothelial cell injury.
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