ArticleThe American journal of pathology2012
Protein kinase G-I deficiency induces pulmonary hypertension through Rho A/Rho kinase activation.
Article in The American journal of pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 40 citations in OpenAlex.
- Endothelial C-type natriuretic peptide/guanylyl cyclase-B signaling prevents pulmonary arterial hypertension.Nature communications · 2026Article
- Genome-wide scan for selection signatures reveals novel insights into the adaptive capacity characteristics in three Chinese cattle breeds.BMC genomics · 2025Article
- Phosphodiesterase 9A inhibition improves aging-related increase in pulmonary vascular resistance in mice.GeroScience · 2024Article
- Endothelial PHD2 deficiency induces nitrative stressThe European respiratory journal · 2022Article
- Mechanosensitive cation currents through TRPC6 and Piezo1 channels in human pulmonary arterial endothelial cells.American journal of physiology. Cell physiology · 2022Article
- Predicting High Blood Pressure Using DNA Methylome-Based Machine Learning Models.Biomedicines · 2022Article
- Hypertension: Potential Player in Cardiovascular Disease Incidence in Preeclampsia.Cardiovascular toxicology · 2022Review
- Tetramethylpyrazine Improves Monocrotaline-Induced Pulmonary Hypertension through the ROS/iNOS/PKG-1 Axis.Journal of healthcare engineering · 2022Article
- Endothelial cells in the pathogenesis of pulmonary arterial hypertension.The European respiratory journal · 2021Review
- HCell death discovery · 2021Article
- Endothelial-to-Mesenchymal Transition in Pulmonary Arterial Hypertension.Antioxidants & redox signaling · 2021Review
- Redox Regulation, Oxidative Stress, and Inflammation in Group 3 Pulmonary Hypertension.Advances in experimental medicine and biology · 2021Review
- Oxidation of PKGIα mediates an endogenous adaptation to pulmonary hypertension.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Therapeutic Targeting of Vascular Remodeling and Right Heart Failure in Pulmonary Arterial Hypertension with a HIF-2α Inhibitor.American journal of respiratory and critical care medicine · 2018Article
- Article
- Reactive Oxygen and Nitrogen Species in the Development of Pulmonary Hypertension.Antioxidants (Basel, Switzerland) · 2017Review
- Regulation of Pulmonary Vascular Smooth Muscle Contractility in Pulmonary Arterial Hypertension: Implications for Therapy.Frontiers in physiology · 2017Review
- Molecular Basis of Nitrative Stress in the Pathogenesis of Pulmonary Hypertension.Advances in experimental medicine and biology · 2017Review
- Update on novel targets and potential treatment avenues in pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2016Review
- Endothelial and Smooth Muscle Cell Interactions in the Pathobiology of Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2016Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Protein kinase G (PKG) plays an important role in the regulation of vascular smooth cell contractility and is a critical mediator of nitric oxide signaling, which regulates cardiovascular homeostasis. PKG-I-knockout (Prkg1(-/-)) mice exhibit impaired nitric oxide/cGMP-dependent vasorelaxation and systemic hypertension. However, it remains unknown whether PKG-I deficiency induces pulmonary hypertension. In this study, we characterized the hypertensive pulmonary phenotypes in Prkg1(-/-) mice and delineated the underlying molecular basis. We observed a significant increase in right ventricular systolic pressure in Prkg1(-/-) mice in the absence of systemic hypertension and left-sided heart dysfunction. In addition, we observed marked muscularization of distal pulmonary vessels in Prkg1(-/-) mice. Microangiography revealed impaired integrity of the pulmonary vasculature in Prkg1(-/-) mice. Mechanistically, PKG-I-mediated phosphorylation of Rho A Ser188 was markedly decreased, and the resultant Rho A activation was significantly increased in Prkg1(-/-) lung tissues, which resulted in Rho kinase activation. The i.t. administration of fasudil, a Rho kinase inhibitor, reversed the hypertensive pulmonary phenotype in Prkg1(-/-) mice. Taken together, these data show that PKG-I deficiency induces pulmonary hypertension through Rho A/Rho kinase activation-mediated vasoconstriction and pulmonary vascular remodeling.
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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.