ArticleFree radical biology & medicine2014
Caveolin-1 is a negative regulator of NADPH oxidase-derived reactive oxygen species.
Article in Free radical biology & medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 60 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
60 citing papers in PubMed, 95 citations in OpenAlex.
- Review
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- The critical roles of caveolin-1 in lung diseases.Frontiers in pharmacology · 2024Review
- A Reappraisal of the Utility of L-012 to Measure Superoxide from Biologically Relevant Sources.Antioxidants (Basel, Switzerland) · 2023Article
- Structure, regulation, and physiological functions of NADPH oxidase 5 (NOX5).Journal of physiology and biochemistry · 2023Review
- Caveolin-3 Nitration Drives Insulin Resistance in Prediabetic Hearts.Circulation · 2023Article
- Calpain Regulates Reactive Oxygen Species Production during Capacitation through the Activation of NOX2 and NOX4.International journal of molecular sciences · 2023Article
- Functional interactions between NADPH oxidase 5 and actin.Frontiers in cell and developmental biology · 2023Article
- Role of autophagy in cancer-associated fibroblast activation, signaling and metabolic reprograming.Frontiers in cell and developmental biology · 2023Review
- Article
- Calmodulin binding to the dehydrogenase domain of NADPH oxidase 5 alters its oligomeric state.Biochemistry and biophysics reports · 2022Article
- Cardiomyocyte Microtubules: Control of Mechanics, Transport, and Remodeling.Annual review of physiology · 2022Review
- Endothelin-1 Induced Phosphorylation of Caveolin-1 and Smad2C in Human Vascular Smooth Muscle Cells: Role of NADPH Oxidases, c-Abl, and Caveolae Integrity in TGF-β Receptor Transactivation.International journal of molecular and cellular medicine · 2022Article
- Protective role of Cav-1 in pneumolysin-induced endothelial barrier dysfunction.Frontiers in immunology · 2022Article
- Multiple subregions within the caveolin-1 scaffolding domain inhibit fibrosis, microvascular leakage, and monocyte migration.PloS one · 2022Article
- Critical Role of Caveolin-1 Loss/Dysfunction in Pulmonary Hypertension.Medical sciences (Basel, Switzerland) · 2021Review
- Nitric oxide and heme-NO stimulate superoxide production by NADPH oxidase 5.Free radical biology & medicine · 2021Article
- The Caveolin-1 Scaffolding Domain Peptide Reverses Aging-Associated Deleterious Changes in Multiple Organs.The Journal of pharmacology and experimental therapeutics · 2021Article
- Sex Dimorphism in Pulmonary Hypertension: The Role of the Sex Chromosomes.Antioxidants (Basel, Switzerland) · 2021Review
Corrections and comments
- Erratum issuedBlack, Stephen M [added]; Rafikov, Ruslan [added]
Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Changes in the expression and function of caveolin-1 (Cav-1) have been proposed as a pathogenic mechanism underlying many cardiovascular diseases. Cav-1 binds to and regulates the activity of numerous signaling proteins via interactions with its scaffolding domain. In endothelial cells, Cav-1 has been shown to reduce reactive oxygen species (ROS) production, but whether Cav-1 regulates the activity of NADPH oxidases (Noxes), a major source of cellular ROS, has not yet been shown. Herein, we show that Cav-1 is primarily expressed in the endothelium and adventitia of pulmonary arteries (PAs) and that Cav-1 expression is reduced in isolated PAs from multiple models of pulmonary artery hypertension (PH). Reduced Cav-1 expression correlates with increased ROS production in the adventitia of hypertensive PA. In vitro experiments revealed a significant ability of Cav-1 and its scaffolding domain to inhibit Nox1-5 activity and it was also found that Cav-1 binds to Nox5 and Nox2 but not Nox4. In addition to posttranslational actions, in primary cells, Cav-1 represses the mRNA and protein expression of Nox2 and Nox4 through inhibition of the NF-κB pathway. Last, in a mouse hypoxia model, the genetic ablation of Cav-1 increased the expression of Nox2 and Nox4 and exacerbated PH. Together, these results suggest that Cav-1 is a negative regulator of Nox function via two distinct mechanisms, acutely through direct binding and chronically through alteration of expression levels. Accordingly, the loss of Cav-1 expression in cardiovascular diseases such as PH may account for the increased Nox activity and greater production of ROS.
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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 OpenQuestion graph.