ArticleThe American journal of pathology2011
Spontaneous lung dysfunction and fibrosis in mice lacking connexin 40 and endothelial cell connexin 43.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 46 citations in OpenAlex.
- Connexin 43 Loss in Endothelial Progenitors Facilitates Functional Airway Adaptation After Lung Injury.Research square · 2026Article
- Inhibitor of PD-1/PD-L1: a new approach may be beneficial for the treatment of idiopathic pulmonary fibrosis.Journal of translational medicine · 2024Review
- Connexin 37, 40, 43 and Pannexin 1 Expression in the Gastric Mucosa of Patients with Systemic Sclerosis.Biomedicines · 2023Article
- Blocking connexin 43 and its promotion of ATP release from renal tubular epithelial cells ameliorates renal fibrosis.Cell death & disease · 2022Article
- Immune Stroma in Lung Cancer and Idiopathic Pulmonary Fibrosis: A Common Biologic Landscape?International journal of molecular sciences · 2021Review
- Ischemia-reperfusion Injury in the Transplanted Lung: A Literature Review.Transplantation direct · 2021Review
- Signaling Pathways Involved in the Development of Bronchopulmonary Dysplasia and Pulmonary Hypertension.Children (Basel, Switzerland) · 2020Review
- Role of phosphatase and tensin homolog in hypoxic pulmonary vasoconstriction.Cardiovascular research · 2017Article
- The role of gap junctions in inflammatory and neoplastic disorders (Review).International journal of molecular medicine · 2017Review
- Alveolar epithelial disintegrity in pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2016Review
- Connexins, Pannexins, and Their Channels in Fibroproliferative Diseases.The Journal of membrane biology · 2016Review
- Immunohisto- and Cytochemistry Analysis of Connexins.Methods in molecular biology (Clifton, N.J.) · 2016Article
- Idiopathic pulmonary fibrosis and cancer: do they really look similar?BMC medicine · 2015Article
- The lung communication network.Cellular and molecular life sciences : CMLS · 2015Review
- Restoration of impaired endothelial myocyte enhancer factor 2 function rescues pulmonary arterial hypertension.Circulation · 2015Article
- The loss of cellular junctions in epithelial lung cells induced by cigarette smoke is attenuated by corilagin.Oxidative medicine and cellular longevity · 2015Article
- Connexin mutant embryonic stem cells and human diseases.World journal of stem cells · 2014Review
- Regulation of cellular communication by signaling microdomains in the blood vessel wall.Pharmacological reviews · 2014Review
- Connexin43 mediates NF-κB signalling activation induced by high glucose in GMCs: involvement of c-Src.Cell communication and signaling : CCS · 2013Article
- Hypoxic pulmonary vasoconstriction requires connexin 40-mediated endothelial signal conduction.The Journal of clinical investigation · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Gap junction proteins (connexins) facilitate intercellular communication and serve several roles in regulation of tissue function and remodeling. To examine the physiologic effects of depleting two prominent endothelial connexins, Cx40 and Cx43, transgenic mice were generated by breeding Cx40-deficient mice (Cx40(-/-)) with a vascular endothelial cell (VEC)-specific Cx43-deficient mouse strain (VEC Cx43(-/-)) to produce double-connexin knockout mice (VEC Cx43(-/-)/Cx40(-/-)). The life span in VEC Cx43(-/-)/Cx40(-/-) mice was dramatically shortened, which correlated with severe spontaneous lung abnormalities as the mice aged including increased fibrosis, aberrant alveolar remodeling, and increased lung fibroblast content. Moreover, VEC Cx43(-/-)/Cx40(-/-) mice exhibited cardiac hypertrophy and hypertension. Because VEC Cx43(-/-)/Cx40(-/-) mice demonstrated phenotypic hallmarks that were remarkably similar to those in mice deficient in caveolin-1, pulmonary caveolin expression was examined. Lungs from VEC Cx43(-/-)/Cx40(-/-) mice demonstrated significantly decreased expression of caveolin-1 and caveolin-2. This suggests that expression of caveolin-1 may be linked to expression of Cx40 and endothelial Cx43. Moreover, the phenotype of caveolin-1(-/-) mice and VEC Cx43(-/-)/Cx40(-/-) mice may arise via a common mechanism.
Indexed as
Identifiers
What OpenQuestion holds
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.