ArticleNature communications2020
Therapeutic potential of KLF2-induced exosomal microRNAs in pulmonary hypertension.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 61 papers.
What it found
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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.
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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.
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Who cites it
61 citing papers in PubMed, 98 citations in OpenAlex.
- KLF6 activation marks an angiogenic and apoptosis resistant endothelial phenotype in pulmonary arterial hypertension.Communications biology · 2026Article
- Expanding the genetic burden of low-evidence genes in pulmonary arterial hypertension.European journal of human genetics : EJHG · 2026Article
- The Role of the Apelin Receptor in the Pathophysiology of Pulmonary Arterial Hypertension.Cells · 2026Review
- Role and relevance of exosome-mediated epigenetic regulation in the pathogenesis, diagnosis and treatment of cardiovascular diseases (Review).Molecular medicine reports · 2026Review
- Engineered MSC-Exosomes Delivering miRNAs for Respiratory Disease Diagnostics and Therapy: Opportunities and Challenges.International journal of nanomedicine · 2026Review
- The Role of Exosomes in Pulmonary Hypertension: Mechanisms and Therapeutic Potential.International journal of nanomedicine · 2026Review
- Targeting Inflammation-Oxidative Stress Crosstalk: Advances and Challenges in Nanocarrier-Based Interventional Strategies for Pulmonary Arterial Hypertension.International journal of nanomedicine · 2026Review
- Intranasal delivery of LB244-loaded M2 microglia membrane nanoparticles for targeted treatment of neuroinflammation after I/R brain injury.Materials today. Bio · 2025Article
- Rewriting the vascular script: epigenetic modifiers as scribes of metabolic reprogramming in pulmonary hypertension.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Pathophysiology of Pulmonary Arterial Hypertension: Focus on Vascular Endothelium as a Potential Therapeutic Target.International journal of molecular sciences · 2025Review
- Article
- The role of lactate metabolism and lactylation in pulmonary arterial hypertension.Respiratory research · 2025Review
- Emerging Gene Therapy Based on Nanocarriers: A Promising Therapeutic Alternative for Cardiovascular Diseases and a Novel Strategy in Valvular Heart Disease.International journal of molecular sciences · 2025Review
- Protective Effects ofBiology · 2025Article
- Unlocking the Potential of Extracellular Vesicles in Cardiovascular Disease.Journal of cellular and molecular medicine · 2025Review
- 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
- Article
- Elevated Shear Stress Modulates Heterogenous Cellular Subpopulations to Induce Vascular Remodeling.Tissue engineering. Part A · 2024Article
- Human Breast Milk Exosomes: Affecting Factors, Their Possible Health Outcomes, and Future Directions in Dietetics.Nutrients · 2024Review
- Harmonising cellular conversations: decoding the vital roles of extracellular vesicles in respiratory system intercellular communications.European respiratory review : an official journal of the European Respiratory Society · 2024Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
18 authors at 9 institutions in 6 countries.
Funding
Abstract
Pulmonary arterial hypertension (PAH) is a severe disorder of lung vasculature that causes right heart failure. Homoeostatic effects of flow-activated transcription factor Krüppel-like factor 2 (KLF2) are compromised in PAH. Here, we show that KLF2-induced exosomal microRNAs, miR-181a-5p and miR-324-5p act together to attenuate pulmonary vascular remodelling and that their actions are mediated by Notch4 and ETS1 and other key regulators of vascular homoeostasis. Expressions of KLF2, miR-181a-5p and miR-324-5p are reduced, while levels of their target genes are elevated in pre-clinical PAH, idiopathic PAH and heritable PAH with missense p.H288Y KLF2 mutation. Therapeutic supplementation of miR-181a-5p and miR-324-5p reduces proliferative and angiogenic responses in patient-derived cells and attenuates disease progression in PAH mice. This study shows that reduced KLF2 signalling is a common feature of human PAH and highlights the potential therapeutic role of KLF2-regulated exosomal miRNAs in PAH and other diseases associated with vascular remodelling.
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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.