ArticleInternational journal of molecular medicine2019
Long non‑coding RNA MALAT1 sponges miR‑124‑3p.1/KLF5 to promote pulmonary vascular remodeling and cell cycle progression of pulmonary artery hypertension.
Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 67 citations in OpenAlex.
- Silencing MALAT1 represses pathological progression, inflammation, and vascular smooth muscle cell phenotype switching by regulating the SEMA3C-mediated Smad pathway in intracranial aneurysms.Frontiers in cellular neuroscience · 2026Article
- Canonical and emerging regulatory mechanisms of tissue remodeling: shared principles across organs and therapeutic opportunities.Frontiers in immunology · 2026Review
- MicroRNAs as Biomarkers for the Diagnosis and Prognosis of Different Diseases and Cancer.Experientia supplementum (2012) · 2026Review
- MicroRNA signature predicts post operative atrial fibrillation after coronary artery bypass grafting.Scientific reports · 2025Article
- Positive Feedback Regulation between KLF5 and XPO1 Promotes Cell Cycle Progression of Basal like Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Ambrisentan Retains Its Pro-Autophagic Activity on Human Pulmonary Artery Endothelial Cells Exposed to Hypoxia in an In Vitro Model Mimicking Diabetes.Journal of cellular and molecular medicine · 2025Article
- Review
- Comprehensive insights and In silico analysis into the emerging role of LincRNAs in lung diseases pathogenesis; a step toward ncRNA precision.Functional & integrative genomics · 2025Review
- Ginsenoside Rg1 Regulates the Activation of Astrocytes Through lncRNA-Malat1/miR-124-3p/Lamc1 Axis Driving PI3K/AKT Signaling Pathway, Promoting the Repair of Spinal Cord Injury.CNS neuroscience & therapeutics · 2024Article
- Roles of LncRNAs in the Pathogenesis of Pulmonary Hypertension.Reviews in cardiovascular medicine · 2024Review
- Long Noncoding RNA MALAT1: Salt-Sensitive Hypertension.International journal of molecular sciences · 2024Review
- Identification and Analysis of Differentially Expressed Genes Associated with Ferroptosis and HIV in PASMCs Based on Bioinformatics.Current HIV research · 2024Article
- Unraveling the epigenetic landscape of pulmonary arterial hypertension: implications for personalized medicine development.Journal of translational medicine · 2023Review
- Hibiscus attenuates renovascular hypertension-induced aortic remodeling dose dependently: the oxidative stress role and Ang II/cyclophilin A/ERK1/2 signaling.Frontiers in physiology · 2023Article
- Emerging role of long non-coding RNA MALAT1 related signaling pathways in the pathogenesis of lung disease.Frontiers in cell and developmental biology · 2023Review
- miR-124-3p sabotages lncRNA MALAT1 stability to repress chondrocyte pyroptosis and relieve cartilage injury in osteoarthritis.Journal of orthopaedic surgery and research · 2022Article
- The Landscape of Noncoding RNA in Pulmonary Hypertension.Biomolecules · 2022Review
- miR-155-5p regulates hypoxia-induced pulmonary artery smooth muscle cell function by targeting PYGL.Bioengineered · 2022Article
- Decrease in LINC00963 attenuates the progression of pulmonary arterial hypertension via microRNA-328-3p/profilin 1 axis.Journal of clinical laboratory analysis · 2022Article
- MicroRNAs in Pulmonary Hypertension, from Pathogenesis to Diagnosis and Treatment.Biomolecules · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have demonstrated that long non‑coding RNA (lncRNA) is involved in vascular remodeling. The metastasis‑associated lung adenocarcinoma transcript 1 (MALAT1) lncRNA is associated with the proliferation and migration of vascular smooth muscle and endothelial cells; however, its biological role in pulmonary artery hypertension (PAH) is currently unclear. The aim of the present study was to investigate the post‑transcriptional regulation of MALAT1 in human pulmonary artery smooth muscle cells (HPASMCs). The results revealed that MALAT1 expression levels were significantly upregulated in the pulmonary arteries (PAs) and HPASMCs obtained from patients with PAH compared with adjacent normal PA tissues and HPASMCs. Knockdown of MALAT1 suppressed the viability and proliferation of HPASMCs and prevented cells entering the G0/G1 cell cycle phase. MALAT1 overexpression exerted the opposite effects. Bioinformatics analysis predicted complementary binding of hsa‑microRNA (miR)‑124‑3p.1 with the 3'‑untranslated region of MALAT1. Luciferase reporter assays and RNA immunoprecipitation experiments demonstrated molecular binding between MALAT1 and hsa‑miR‑124‑3p.1. This resulted in the formation of an RNA‑induced silencing complex. In addition, Kruppel‑like factor 5 (KLF5) was confirmed to be a target gene of MALAT1/hsa‑miR‑124‑3p.1. MALAT1 silencing did not inhibit the proliferation and migration of HPASMCs following knockdown of hsa‑miR‑124‑3p.1. In addition, MALAT1 knockdown was demonstrated to attenuate the expression of KLF5. Following MALAT1 knockdown, the expression level of KLF5 was rescued by inhibition of hsa‑miR‑124‑3p.1 expression. The results of the current study indicate that the MALAT1/hsa‑miR‑124‑3p.1/KLF5 axis may serve a key role in HPASMCs. In addition, the results contribute to what is known regarding the role of MALAT1 in PAH development and provide a novel theoretical basis for the development of new therapeutic interventions for patients with PAH.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.