ReviewJournal of molecular medicine (Berlin, Germany)2007
Connexin37: a potential modifier gene of inflammatory disease.
Review in Journal of molecular medicine (Berlin, Germany), 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 40 citations in OpenAlex.
- Connexin 37 Regulates the Kv1.3 Pathway and Promotes the Development of Atherosclerosis.Mediators of inflammation · 2022Article
- The role of connexin 37 polymorphism in spontaneous abortion.Physiological research · 2021Article
- Serine 319 phosphorylation is necessary and sufficient to induce a Cx37 conformation that leads to arrested cell cycling.Journal of cell science · 2020Article
- Interaction betweenExperimental biology and medicine (Maywood, N.J.) · 2019Article
- The relationship between insulin resistance, adiponectin and C-reactive protein and vascular endothelial injury in diabetic patients with coronary heart disease.Experimental and therapeutic medicine · 2018Article
- Polymorphism of CONNEXIN37 gene is a risk factor for ischemic stroke in Han Chinese population.Lipids in health and disease · 2018Article
- High bone mass in mice lacking Cx37 because of defective osteoclast differentiation.The Journal of biological chemistry · 2014Article
- Gap junction protein Cx37 interacts with endothelial nitric oxide synthase in endothelial cells.Arteriosclerosis, thrombosis, and vascular biology · 2010Article
- Molecular genetics of atherosclerosis.Human genetics · 2009Review
- Connexins participate in the initiation and progression of atherosclerosis.Seminars in immunopathology · 2009Review
- Biological and biophysical properties of vascular connexin channels.International review of cell and molecular biology · 2009Review
- Remodeling of cardiac fibroblasts following myocardial infarction results in increased gap junction intercellular communication.Cardiovascular pathology : the official journal of the Society for Cardiovascular PathologyArticle
- Connexins and their channels in inflammation.Critical reviews in biochemistry and molecular biologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is an increasing appreciation of the importance of gap junction proteins (connexins) in modulating the severity of inflammatory diseases. Multiple epidemiological gene association studies have detected a link between a single nucleotide polymorphism in the human connexin37 (Cx37) gene and coronary artery disease or myocardial infarction in various populations. This C1019T polymorphism causes a proline-to-serine substitution (P319S) in the regulatory C terminal tail of Cx37, a protein that is expressed in the vascular endothelium as well as in monocytes and macrophages. Indeed, these three cell types are key players in atherogenesis. In the early phases of atherosclerosis, blood monocytes are recruited to the sites of injury in response to chemotactic factors. Monocytes adhere to the dysfunctional endothelium and transmigrate across endothelial cells to penetrate the arterial intima. In the intima, monocytes proliferate, mature, and accumulate lipids to progress into macrophage foam cells. This review focuses on Cx37 and its impact on the cellular and molecular events underlying tissue function, with particular emphasis of the contribution of the C1019T polymorphism in atherosclerosis. We will also discuss evidence for a potential mechanism by which allelic variants of Cx37 are differentially predictive of increased risk for inflammatory diseases.
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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.