ArticleInternational journal of molecular sciences2024
Unraveling the Impact of miR-146a in Pulmonary Arterial Hypertension Pathophysiology and Right Ventricular Function.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Circulating microRNAs in pulmonary arterial hypertension: biomarkers for diagnosis, prognostic stratification, and treatment.GeroScience · 2026Review
- The Role of the Apelin Receptor in the Pathophysiology of Pulmonary Arterial Hypertension.Cells · 2026Review
- MicroRNA-661 Suppresses Proliferation and Migration of Pulmonary Artery Smooth Muscle Cells and Endothelial Cells by Targeting CCND2.Biologics : targets & therapy · 2026Article
- miRNAs in Pulmonary Hypertension: Mechanistic Insights and Therapeutic Potential.Biomedicines · 2025Review
- Utilizing Circulating MicroRNAs for Personalized Exercise Programs: Insights into Physiological Adaptations and Individual Responses.Iranian journal of biotechnology · 2025Review
- 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
- miRNA regulatory networks as precision diagnostic and therapeutic targets in pulmonary arterial hypertension: from molecular cascades to clinical translation.American journal of cardiovascular disease · 2025Review
- Lymphocyte Involvement in the Pathology of Pulmonary Arterial Hypertension.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
Pulmonary arterial hypertension (PAH) is a chronic disorder characterized by excessive pulmonary vascular remodeling, leading to elevated pulmonary vascular resistance and right ventricle (RV) overload and failure. MicroRNA-146a (miR-146a) promotes vascular smooth muscle cell proliferation and vascular neointimal hyperplasia, both hallmarks of PAH. This study aimed to investigate the effects of miR-146a through pharmacological or genetic inhibition on experimental PAH and RV pressure overload animal models. Additionally, we examined the overexpression of miR-146a on human pulmonary artery smooth muscle cells (hPASMCs). Here, we showed that miR-146a genic expression was increased in the lungs of patients with PAH and the plasma of monocrotaline (MCT) rats. Interestingly, genetic ablation of miR-146a improved RV hypertrophy and systolic pressures in Sugen 5415/hypoxia (SuHx) and pulmonary arterial banding (PAB) mice. Pharmacological inhibition of miR-146a improved RV remodeling in PAB-wild type mice and MCT rats, and enhanced exercise capacity in MCT rats. However, overexpression of miR-146a did not affect proliferation, migration, and apoptosis in control-hPASMCs. Our findings show that miR-146a may play a significant role in RV function and remodeling, representing a promising therapeutic target for RV hypertrophy and, consequently, PAH.
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Registered trials
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