ArticleNature communications2019
Targeting cyclin-dependent kinases for the treatment of pulmonary arterial hypertension.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.
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Who cites it
54 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.
- Searching for Old and New Small-Molecule Protein Kinase Inhibitors as Effective Treatments in Pulmonary Hypertension-A Systematic Review.International journal of molecular sciences · 2024Pooled it
- VITAGRAPH: building a knowledge graph for biologically relevant learning tasks.Scientific data · 2026Article
- Multi-Omic and Single-Cell Approaches for Elucidating Cell Biology and Pathobiology of Lung Disease.American journal of respiratory cell and molecular biology · 2026Review
- Cellular senescence in adult pulmonary hypertension: current state and future challenges.European respiratory review : an official journal of the European Respiratory Society · 2025Review
- Unraveling AURKB as a potential therapeutic target in pulmonary hypertension using integrated transcriptomic analysis and pre-clinical studies.Cell reports. Medicine · 2025Article
- Deciphering the role of miRNA-mRNA interactions in cerebral vasospasm post intracranial hemorrhage.Frontiers in molecular biosciences · 2025Article
- Integrative Multiomics in the Lung Reveals a Protective Role of Asporin in Pulmonary Arterial Hypertension.Circulation · 2024Article
- miR-30d Attenuates Pulmonary Arterial Hypertension via Targeting MTDH and PDE5A and Modulates the Beneficial Effect of Sildenafil.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Dysregulation of the Long Noncoding RNA X-Inactive-Specific Transcript Expression in Male Patients with Pulmonary Arterial Hypertension.The American journal of pathology · 2024Article
- Transcriptomic profiling highlights cell proliferation in the progression of experimental pulmonary hypertension in rats.Scientific reports · 2024Article
- Does Cell-Type-Specific Silencing of Monoamine Oxidase B Interfere with the Development of Right Ventricle (RV) Hypertrophy or Right Ventricle Failure in Pulmonary Hypertension?International journal of molecular sciences · 2024Article
- Protein-protein interaction network-based integration of GWAS and functional data for blood pressure regulation analysis.Human genomics · 2024Article
- Alveolar macrophage-expressed Plet1 is a driver of lung epithelial repair after viral pneumonia.Nature communications · 2024Article
- Pneumococcal hydrogen peroxide regulates host cell kinase activity.Frontiers in immunology · 2024Article
- Mediating oxidative stress through the Palbociclib/miR-141-3p/STAT4 axis in osteoporosis: a bioinformatics and experimental validation study.Scientific reports · 2023Article
- DRU-Net: Pulmonary Artery Segmentation via Dense Residual U-Network with Hybrid Loss Function.Sensors (Basel, Switzerland) · 2023Article
- Flavopiridol Mitigates the Progression of Monocrotaline-Induced Pulmonary Hypertension in Rats by Targeting Cyclin-Dependent Kinase 9.Cardiovascular drugs and therapy · 2023Article
- Article
- Current understanding of the contribution of lactate to the cardiovascular system and its therapeutic relevance.Frontiers in endocrinology · 2023Article
- Transcription factors and potential therapeutic targets for pulmonary hypertension.Frontiers in cell and developmental biology · 2023Review
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary arterial hypertension (PAH) is a devastating disease with poor prognosis and limited therapeutic options. We screened for pathways that may be responsible for the abnormal phenotype of pulmonary arterial smooth muscle cells (PASMCs), a major contributor of PAH pathobiology, and identified cyclin-dependent kinases (CDKs) as overactivated kinases in specimens derived from patients with idiopathic PAH. This increased CDK activity is confirmed at the level of mRNA and protein expression in human and experimental PAH, respectively. Specific CDK inhibition by dinaciclib and palbociclib decreases PASMC proliferation via cell cycle arrest and interference with the downstream CDK-Rb (retinoblastoma protein)-E2F signaling pathway. In two experimental models of PAH (i.e., monocrotaline and Su5416/hypoxia treated rats) palbociclib reverses the elevated right ventricular systolic pressure, reduces right heart hypertrophy, restores the cardiac index, and reduces pulmonary vascular remodeling. These results demonstrate that inhibition of CDKs by palbociclib may be a therapeutic strategy in PAH.
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