Evidence map›Paper›PMID 18834327›Full record

ReviewAntioxidants & redox signaling2009

Connexins in vascular physiology and pathology.

Anne C Brisset, Brant E Isakson, Brenda R Kwak

Open access · greenAbstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
5.9field-weighted citation impact, top 3% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

73 citing papers in PubMed, 175 citations in OpenAlex.

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13 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 2 countries.

Anne C BrissetDivision of Cardiology, Geneva University Hospitals, Geneva, Switzerland.
Brant E Isakson
Brenda R Kwak
University Hospital of Geneva · CHUniversity of Virginia · US

Funding

Mechanisms of Heterocellular Signaling at the Myoenothelial JunctionR01HL088554 · NHLBI · UNIVERSITY OF VIRGINIA · PI ISAKSON, BRANT E, WEISS, MITCHELL J · 2008 to 2017
$3.8M
NHLBI NIH HHS HL88554NHLBI NIH HHS R01 HL088554
6 · The paper itself

Abstract

Cellular interaction in blood vessels is maintained by multiple communication pathways, including gap junctions. They consist of intercellular channels ensuring direct interaction between endothelial and smooth muscle cells and the synchronization of their behavior along the vascular wall. Gap-junction channels arise from the docking of two hemichannels or connexons, formed by the assembly of six connexins, and achieve direct cellular communication by allowing the transport of small metabolites, second messengers, and ions between two adjacent cells. Physiologic variations in connexin expression are observed along the vascular tree, with most common connexins being Cx37, Cx40, and Cx43. Changes in the level of expression of connexins have been correlated to the development of vascular disease, such as hypertension, atherosclerosis, or restenosis. Recent studies on connexin-deficient mice highlighted key roles of these communication pathways in the development of these pathologies and confirmed the need for targeted pharmacologic approaches for their prevention and treatment. The aim of this issue is to review the current knowledge on the implication of gap junctions in vascular function and most common cardiovascular diseases.

Indexed as

AnimalsCell CommunicationConnexinsEndothelium, VascularGap JunctionsHumansMiceMuscle, Smooth, VascularVascular DiseasesConnexins

Identifiers

PMID18834327
PMCPMC2819334
OpenAlexW2119108045

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.