ArticlePulmonary circulation2013
Nitrosation-dependent caveolin 1 phosphorylation, ubiquitination, and degradation and its association with idiopathic pulmonary arterial hypertension.
Article in Pulmonary circulation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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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Who cites it
52 citing papers in PubMed, 69 citations in OpenAlex.
- RNF213 in Panvascular Disease: A Molecular Hub Linking Genetic Susceptibility to Systemic Vasculopathy.Biomedicines · 2026Review
- Caveolae mechanics in cellular functions and disease.Nature reviews. Molecular cell biology · 2026Review
- Caveolin-1 Is a Central Mediator of Acute Lung Injury in an Animal Model of Sickle Cell Disease.Pulmonary circulation · 2025Article
- Nitrosation of CD36 Regulates Endothelial Function and Serum Lipids.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Increased antioxidative defense and reduced advanced glycation end-product formation by metabolic adaptation in non-small-cell-lung-cancer patients.Nature communications · 2025Article
- USP11 Promotes Endothelial Apoptosis-Resistance in Pulmonary Arterial Hypertension by Deubiquitinating HINT3.Journal of respiratory biology and translational medicine · 2025Article
- Subcellular Localization Guides eNOS Function.International journal of molecular sciences · 2024Review
- ROS-mediated regulation of β2AR function: Does oxidation play a meaningful role towards β2-agonist tachyphylaxis in airway obstructive diseases?Biochemical pharmacology · 2024Review
- Physiological and pathological roles of caveolins in the central nervous system.Trends in neurosciences · 2024Review
- The purified extract of steamedJournal of ginseng research · 2023Article
- Adiposomes from Obese-Diabetic Individuals Promote Endothelial Dysfunction and Loss of Surface Caveolae.Cells · 2023Article
- Reduced endothelial caveolin-1 underlies deficits in brain insulin signalling in type 2 diabetes.Brain : a journal of neurology · 2023Article
- Using evolutionary data to make sense of macromolecules with a "face-lifted" ConSurf.Protein science : a publication of the Protein Society · 2023Article
- Caveolin-1 in vascular health and glaucoma: A critical vascular regulator and potential therapeutic target.Frontiers in medicine · 2023Review
- Schistosomiasis-associated pulmonary hypertension unveils disrupted murine gut-lung microbiome and reduced endoprotective Caveolin-1/BMPR2 expression.Frontiers in immunology · 2023Article
- Physiological and pathophysiological mechanisms of the molecular and cellular biology of angiogenesis and inflammation in moyamoya angiopathy and related vascular diseases.Frontiers in neurology · 2023Review
- Cysteine Oxidation Promotes Dimerization/Oligomerization of Circadian Protein Period 2.Biomolecules · 2022Article
- The manifold roles of protein S-nitrosylation in the life of insulin.Nature reviews. Endocrinology · 2022Review
- Ring Finger Protein 213 in Moyamoya Disease With Pulmonary Arterial Hypertension: A Mini-Review.Frontiers in neurology · 2022Review
- Critical Role of Caveolin-1 Loss/Dysfunction in Pulmonary Hypertension.Medical sciences (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 3 countries.
Funding
Abstract
In the present study, we tested the hypothesis that chronic inflammation and oxidative/nitrosative stress induce caveolin 1 (Cav-1) degradation, providing an underlying mechanism of endothelial cell activation/dysfunction and pulmonary vascular remodeling in patients with idiopathic pulmonary arterial hypertension (IPAH). We observed reduced Cav-1 protein despite increased Cav-1 messenger RNA expression and also endothelial nitric oxide synthase (eNOS) hyperphosphorylation in human pulmonary artery endothelial cells (PAECs) from patients with IPAH. In control human lung endothelial cell cultures, tumor necrosis factor α-induced nitric oxide (NO) production and S-nitrosation (SNO) of Cav-1 Cys-156 were associated with Src displacement and activation, Cav-1 Tyr-14 phosphorylation, and destabilization of Cav-1 oligomers within 5 minutes that could be blocked by eNOS or Src inhibition. Prolonged stimulation (72 hours) with NO donor DETANONOate reduced oligomerized and total Cav-1 levels by 40%-80%, similar to that observed in IPAH patient-derived PAECs. NO donor stimulation of endothelial cells for >72 hours, which was associated with sustained Src activation and Cav-1 phosphorylation, ubiquitination, and degradation, was blocked by NOS inhibitor L-NAME, Src inhibitor PP2, and proteosomal inhibitor MG132. Thus, chronic inflammation, sustained eNOS and Src signaling, and Cav-1 degradation may be important causal factors in the development of IPAH by promoting PAEC dysfunction/activation via sustained oxidative/nitrosative stress.
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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 Socratic graph.