Evidence map›Paper›PMID 20155481›Full record

ReviewCellular and molecular life sciences : CMLS2010

Spontaneous arterial dissection: phenotype and molecular pathogenesis.

Caspar Grond-Ginsbach, Rastislav Pjontek, Suna Su Aksay, Alexander Hyhlik-Dürr, Dittmar Böckler, Marie-Luise Gross-Weissmann

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 54 citations in OpenAlex.

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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

6 authors at 1 institution in 2 countries.

Caspar Grond-GinsbachDepartment of Neurology, University of Heidelberg, Heidelberg, Germany. Caspar.Grond-Ginsbach@med.uni-heidelberg.de
Rastislav Pjontek
Suna Su Aksay
Alexander Hyhlik-Dürr
Dittmar Böckler
Marie-Luise Gross-Weissmann
Heidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Arterial dissection (AD) is defined as the longitudinal splitting up of the arterial wall caused by intramural bleeding. It can occur as a spontaneous event in all large and medium sized arteries. The histological hallmark of AD is medial degeneration. Histological investigations, gene expression profiling and proteome studies of affected arteries reveal disturbances in many different biological processes including inflammation, proteolytic activity, cell proliferation, apoptosis and smooth muscle cell (SMC) contractile function. Medial degeneration can be caused by various rare dominant Mendelian disorders. Genetic linkage analysis lead to the identification of mutations in different disease-causing genes involved in the biosynthesis of the extracellular matrix (FBN1, COL3A1), in transforming growth factor (TGF) beta signaling (FBN1, TGFBR1, TGFBR2) and in the SMC contractile system (ACTA2, MYH11). Genome wide association studies suggest that the CDKN2A/CDKN2B locus plays a role in the etiology AD and other arterial diseases.

Indexed as

AnimalsAortic DissectionFemaleGene Expression ProfilingGenetic Predisposition to DiseaseHumansMaleModels, CardiovascularMutationMyocytes, Smooth MusclePeptide HydrolasesPhenotypeTransforming Growth Factor betaPeptide HydrolasesTransforming Growth Factor beta

Identifiers

PMID20155481
PMCPMC11115591
OpenAlexW2077510229

What OpenQuestion holds

Textmetadata
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.