Evidence map›Paper›PMID 31175858›Full record

ReviewJournal of molecular and cellular cardiology2019

Clinical-pathological correlations of BAV and the attendant thoracic aortopathies. Part 2: Pluridisciplinary perspective on their genetic and molecular origins.

Ares Pasipoularides

Open access · greenAbstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.2field-weighted citation impact, top 45% 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

7 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Observational
  5. Article
  6. Observational
  7. Review
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

1 author at 1 institution in 1 country.

Ares PasipoularidesDuke/NSF Center for Emerging Cardiovascular Technologies, Emeritus Faculty of Surgery and of Biomedical Engineering, Duke University School of Medicine and Graduate School, Durham, NC, USA. Electronic address: apasipou@duke.edu.
Duke University · US

Funding

NEW MODELS OF RV DIASTOLIC FUNCTION IN HEART FAILURER01HL050446 · NHLBI · DUKE UNIVERSITY · PI PASIPOULARIDES, ARES · 1995 to 1997
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NHLBI NIH HHS R01 HL050446
6 · The paper itself

Abstract

Bicuspid aortic valve (BAV) arises during valvulogenesis when 2 leaflets/cusps of the aortic valve (AOV) are fused together. Its clinical manifestations pertain to faulty AOV function, the associated aortopathy, and other complications surveyed in Part 1 of the present bipartite-series. Part 2 examines mainly genetic and epigenetic causes of BAV and BAV-associated aortopathies (BAVAs) and disease syndromes (BAVD). Part 1 explored the heterogeneity among subsets of patients with BAV and BAVA/BAVD, and investigated abnormal fluid dynamic stress and strain patterns sustained by the cusps. Specific BAV morphologies engender systolic outflow asymmetries, associated with abnormal aortic regional wall-shear-stress distributions and the expression/localization of BAVAs. Understanding fluid dynamic factors besides the developmental mechanisms and underlying genetics governing these congenital anomalies is necessary to explain patient predisposition to aortopathy and phenotypic heterogeneity. BAV aortopathy entails complex/multifactorial pathophysiology, involving alterations in genetics, epigenetics, hemodynamics, and in cellular and molecular pathways. There is always an interdependence between organismic developmental signals and genes-no systemic signals, no gene-expression; no active gene, no next step. An apposite signal induces the expression of the next developmental gene, which needs be expressed to trigger the next signal, and so on. Hence, embryonic, then post-partum, AOV and thoracic aortic development comprise cascades of developmental genes and their regulation. Interdependencies between them arise, entailing reciprocal/cyclical mutual interactions and adaptive feedback loops, by which developmental morphogenetic processes self-correct responding to environmental inputs/reactions. This Survey can serve as a reference point and driver for further pluridisciplinary BAV/BAVD studies and their clinical translation.

Indexed as

AnimalsAortic Aneurysm, ThoracicAortic ValveBicuspid Aortic Valve DiseaseEpigenesis, GeneticGenotypeHeart Valve DiseasesHigh-Throughput Nucleotide SequencingHumansInheritance PatternsMicePhenotypeTranscriptomeBAV-aortopathyBAV-associated syndromes or diseaseBicuspid aortic valve (BAV)Congenital cardiovascular diseaseExtracellular matrixGenetic screeningNGSPolygenic/multifactorial complex-disease traitsThoracic aortic dilatationsValvulogenesisVascular smooth muscle cell

Identifiers

PMID31175858
PMCPMC6688480
OpenAlexW2952287628

What OpenQuestion holds

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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.