ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015
The reversal of pulmonary vascular remodeling through inhibition of p38 MAPK-alpha: a potential novel anti-inflammatory strategy in pulmonary hypertension.
Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 66 citations in OpenAlex.
- A Plant-Based Diet Alleviates Molecular Pulmonary Abnormalities in Hypertension.Advances in respiratory medicine · 2025Article
- Signaling pathways and targeted therapy for pulmonary hypertension.Signal transduction and targeted therapy · 2025Review
- Pulmonary hypertension: etiology and anti-inflammatory treatment pathways of natural products.Frontiers in pharmacology · 2025Review
- Elevated Shear Stress Modulates Heterogenous Cellular Subpopulations to Induce Vascular Remodeling.Tissue engineering. Part A · 2024Article
- Cellular senescence in the pathogenesis of pulmonary arterial hypertension: the good, the bad and the uncertain.Frontiers in immunology · 2024Review
- Comprehensive analysis of mEpigenetics · 2023Article
- Carbon dioxide and MAPK signalling: towards therapy for inflammation.Cell communication and signaling : CCS · 2023Review
- S100 proteins in cardiovascular diseases.Molecular medicine (Cambridge, Mass.) · 2023Review
- Pulmonary Vascular Remodeling in Pulmonary Hypertension.Journal of personalized medicine · 2023Review
- Interleukin-6 and pulmonary hypertension: from physiopathology to therapy.Frontiers in immunology · 2023Review
- Immunolocalization of zinc transporters and metallothioneins reveals links to microvascular morphology and functions.Histochemistry and cell biology · 2022Article
- Novel p38 Mitogen-Activated Protein Kinase Inhibitor Reverses Hypoxia-Induced Pulmonary Arterial Hypertension in Rats.Pharmaceuticals (Basel, Switzerland) · 2022Article
- The Impact of Sex Chromosomes in the Sexual Dimorphism of Pulmonary Arterial Hypertension.The American journal of pathology · 2022Review
- Endothelial Senescence: A New Age in Pulmonary Hypertension.Circulation research · 2022Review
- The Role of Gut and Airway Microbiota in Pulmonary Arterial Hypertension.Frontiers in microbiology · 2022Review
- Network Pharmacology and Molecular Docking Analysis of Shufeiya Recipe in the Treatment of Pulmonary Hypertension.BioMed research international · 2022Article
- Review
- Therapeutic Potential of Regorafenib-A Multikinase Inhibitor in Pulmonary Hypertension.International journal of molecular sciences · 2021Article
- Review
- p38 MAPK inhibition: A promising therapeutic approach for COVID-19.Journal of molecular and cellular cardiology · 2020Article
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The p38 mitogen-activated protein kinase (MAPK) system is increasingly recognized as an important inflammatory pathway in systemic vascular disease but its role in pulmonary vascular disease is unclear. Previous in vitro studies suggest p38 MAPKα is critical in the proliferation of pulmonary artery fibroblasts, an important step in the pathogenesis of pulmonary vascular remodeling (PVremod). In this study the role of the p38 MAPK pathway was investigated in both in vitro and in vivo models of pulmonary hypertension and human disease. Pharmacological inhibition of p38 MAPKα in both chronic hypoxic and monocrotaline rodent models of pulmonary hypertension prevented and reversed the pulmonary hypertensive phenotype. Furthermore, with the use of a novel and clinically available p38 MAPKα antagonist, reversal of pulmonary hypertension was obtained in both experimental models. Increased expression of phosphorylated p38 MAPK and p38 MAPKα was observed in the pulmonary vasculature from patients with idiopathic pulmonary arterial hypertension, suggesting a role for activation of this pathway in the PVremod A reduction of IL-6 levels in serum and lung tissue was found in the drug-treated animals, suggesting a potential mechanism for this reversal in PVremod. This study suggests that the p38 MAPK and the α-isoform plays a pathogenic role in both human disease and rodent models of pulmonary hypertension potentially mediated through IL-6. Selective inhibition of this pathway may provide a novel therapeutic approach that targets both remodeling and inflammatory pathways in pulmonary vascular disease.
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