ArticleAmerican journal of physiology. Lung cellular and molecular physiology2017
Inflammation-induced caveolin-1 and BMPRII depletion promotes endothelial dysfunction and TGF-β-driven pulmonary vascular remodeling.
Article in American journal of physiology. Lung cellular and molecular physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
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Who cites it
41 citing papers in PubMed, 57 citations in OpenAlex.
- Post-translational modification crosstalk in pulmonary arterial hypertension: mechanisms and therapeutic implications.Molecular biology reports · 2026Review
- Cellular Signalling Networks in High Altitude Pulmonary Hypertension: From Canonical Pathways to Emerging Targets.Cell proliferation · 2026Review
- Macrophage spatiotemporal plasticity in pulmonary diseases: decoding the niche at single-cell resolution.Frontiers in immunology · 2026Review
- Senescent fibroblasts modulate the radiation response of neighboring epithelial cells.Cell death discovery · 2025Article
- Scaffolds with spatiotemporally controlled growth factor delivery and cyclodextrin-enabled antagonism of growth factor receptor sequestration promote cutaneous wound healing.NPJ Regenerative medicine · 2025Article
- Liver bypass in the development of pathogen-associated pulmonary vascular disease: contribution of mesocaval and portosystemic shunts.American journal of physiology. Gastrointestinal and liver physiology · 2025Review
- Precision Medicine for Pulmonary Vascular Disease: The Future Is Now (2023 Grover Conference Series).Pulmonary circulation · 2025Article
- Genetic Manipulation of Caveolin-1 in a Transgenic Mouse Model of Aortic Root Aneurysm: Sex-Dependent Effects on Endothelial and Smooth Muscle Function.International journal of molecular sciences · 2024Article
- Novel insights into the potential applications of stem cells in pulmonary hypertension therapy.Respiratory research · 2024Review
- TGF-β1, pSmad-2/3, Smad-7, and β-Catenin Are Augmented in the Pulmonary Arteries from Patients with Idiopathic Pulmonary Fibrosis (IPF): Role in Driving Endothelial-to-Mesenchymal Transition (EndMT).Journal of clinical medicine · 2024Article
- The critical roles of caveolin-1 in lung diseases.Frontiers in pharmacology · 2024Review
- Induction of CX3CL1 expression by LPS and its impact on invasion and migration in oral squamous cell carcinoma.Frontiers in cell and developmental biology · 2024Article
- Physiological functions of caveolae in endothelium.Current opinion in physiology · 2023Article
- The vascular perspective on acute and chronic lung disease.The Journal of clinical investigation · 2023Review
- Reduced endothelial caveolin-1 underlies deficits in brain insulin signalling in type 2 diabetes.Brain : a journal of neurology · 2023Article
- Role of macrophages in pulmonary arterial hypertension.Frontiers in immunology · 2023Review
- Schistosomiasis-associated pulmonary hypertension unveils disrupted murine gut-lung microbiome and reduced endoprotective Caveolin-1/BMPR2 expression.Frontiers in immunology · 2023Article
- Caveolar and non-Caveolar Caveolin-1 in ocular homeostasis and disease.Progress in retinal and eye research · 2022Review
- Hypoxia-induced pulmonary hypertension upregulates eNOS and TGF-β contributing to sex-linked differences inPulmonary circulation · 2022Article
- Insights on the Gut-Mesentery-Lung Axis in Pulmonary Arterial Hypertension: A Poorly Investigated Crossroad.Arteriosclerosis, thrombosis, and vascular biology · 2022Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Endothelial cell (EC) activation and vascular injury are hallmark features of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Caveolin-1 (Cav-1) is highly expressed in pulmonary microvascular ECs and plays a key role in maintaining vascular homeostasis. The aim of this study was to determine if the lung inflammatory response to
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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.