ArticleAmerican journal of physiology. Heart and circulatory physiology2009
Inhibition of p38 MAPK reverses hypoxia-induced pulmonary artery endothelial dysfunction.
Article in American journal of physiology. Heart and circulatory physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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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Who cites it
22 citing papers in PubMed, 44 citations in OpenAlex.
- Flavonoids: Potential New Drug Candidates for Attenuating Vascular Remodeling in Pulmonary Hypertension.International journal of molecular sciences · 2025Review
- Article
- Cellular senescence in the pathogenesis of pulmonary arterial hypertension: the good, the bad and the uncertain.Frontiers in immunology · 2024Review
- Network Pharmacology and Molecular Docking Analysis of Shufeiya Recipe in the Treatment of Pulmonary Hypertension.BioMed research international · 2022Article
- Paeoniflorin attenuates monocrotaline-induced pulmonary arterial hypertension in rats by suppressing TAK1-MAPK/NF-κB pathways.International journal of medical sciences · 2022Article
- Review
- The Disruption of the Endothelial Barrier Contributes to Acute Lung Injury Induced byInternational journal of molecular sciences · 2021Article
- Protective Effect of Astragaloside IV on High Glucose-Induced Endothelial Dysfunction via Inhibition of P2X7R Dependent P38 MAPK Signaling Pathway.Oxidative medicine and cellular longevity · 2020Article
- YC-1 Prevents Tumor-Associated Tissue Factor Expression and Procoagulant Activity in Hypoxic Conditions by Inhibiting p38/NF-κB Signaling Pathway.International journal of molecular sciences · 2019Article
- Chronic intermittent hypobaric hypoxia attenuates monocrotaline-induced pulmonary arterial hypertension via modulating inflammation and suppressing NF-κB/p38 pathway.Iranian journal of basic medical sciences · 2018Article
- Protein kinase Cα stimulates hypoxia‑induced pulmonary artery smooth muscle cell proliferation in rats through activating the extracellular signal‑regulated kinase 1/2 pathway.Molecular medicine reports · 2017Article
- Involvement of CaBioscience reports · 2017Article
- Leukotriene B4 Activates Pulmonary Artery Adventitial Fibroblasts in Pulmonary Hypertension.Hypertension (Dallas, Tex. : 1979) · 2015Article
- The reversal of pulmonary vascular remodeling through inhibition of p38 MAPK-alpha: a potential novel anti-inflammatory strategy in pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- Enhanced p22phox expression impairs vascular function through p38 and ERK1/2 MAP kinase-dependent mechanisms in type 2 diabetic mice.American journal of physiology. Heart and circulatory physiology · 2014Article
- Chronic hypoxia promotes pulmonary artery endothelial cell proliferation through H2O2-induced 5-lipoxygenase.PloS one · 2014Article
- Altered MAPK signaling in progressive deterioration of endothelial function in diabetic mice.Diabetes · 2012Article
- Reactive oxygen and nitrogen species in pulmonary hypertension.Free radical biology & medicine · 2012Review
- The protective role of 5-hydroxymethyl-2-furfural (5-HMF) against acute hypobaric hypoxia.Cell stress & chaperones · 2011Article
- Increased platelet, leukocyte and endothelial microparticles predict enhanced coagulation and vascular inflammation in pulmonary hypertension.Journal of thrombosis and thrombolysis · 2011Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Hypoxia-induced endothelial dysfunction plays a crucial role in the pathogenesis of hypoxic pulmonary hypertension. p38 MAPK expression is increased in the pulmonary artery following hypoxic exposure. Recent evidence suggests that increased p38 MAPK activity is associated with endothelial dysfunction. However, the role of p38 MAPK activation in pulmonary artery endothelial dysfunction is not known. Sprague-Dawley rats were exposed to 2 wk hypobaric hypoxia, which resulted in the development of pulmonary hypertension and vascular remodeling. Endothelium-dependent relaxation of intrapulmonary vessels from hypoxic animals was impaired due to a reduced nitric oxide (NO) generation. This was despite increased endothelial NO synthase immunostaining and protein expression. Hypoxia exposure increased superoxide generation and p38 MAPK expression. The inhibition of p38 MAPK restored endothelium-dependent relaxation, increased bioavailable NO, and reduced superoxide production. In conclusion, the pharmacological inhibition of p38 MAPK was effective in increasing NO generation, reducing superoxide burden, and restoring hypoxia-induced endothelial dysfunction in rats with hypoxia-induced pulmonary hypertension. p38 MAPK may be a novel target for the treatment of pulmonary hypertension.
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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.