Evidence map›Paper›PMID 27023351›Full record

ArticlePflugers Archiv : European journal of physiology2016

Smooth muscle filamin A is a major determinant of conduit artery structure and function at the adult stage.

Kevin Retailleau, Malika Arhatte, Sophie Demolombe, Martine Jodar, Véronique Baudrie, Stefan Offermanns, Yuanyi Feng, Amanda Patel, Eric Honoré, Fabrice Duprat

Abstract read
PubMed Publisher
In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

14 citing papers in PubMed, 25 citations in OpenAlex.

  1. Relationship BetweenJournal of the American Heart Association · 2025
    Article
  2. Review
  3. Vascular mechanotransduction.Physiological reviews · 2023
    Review
  4. Article
  5. Filamin A Regulates Cardiovascular Remodeling.International journal of molecular sciences · 2021
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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

10 authors at 6 institutions in 3 countries.

Kevin RetailleauInstitut de Pharmacologie Moléculaire et Cellulaire, LabEx ICST, UMR 7275 CNRS, Université de Nice Sophia Antipolis, Valbonne, France.
Malika ArhatteInstitut de Pharmacologie Moléculaire et Cellulaire, LabEx ICST, UMR 7275 CNRS, Université de Nice Sophia Antipolis, Valbonne, France.
Sophie DemolombeInstitut de Pharmacologie Moléculaire et Cellulaire, LabEx ICST, UMR 7275 CNRS, Université de Nice Sophia Antipolis, Valbonne, France.
Martine JodarInstitut de Pharmacologie Moléculaire et Cellulaire, LabEx ICST, UMR 7275 CNRS, Université de Nice Sophia Antipolis, Valbonne, France.
Véronique BaudrieINSERM U970, PARCC-Université Paris Descartes-Hôpital Européen Georges Pompidou, AP-HP, Paris, 75015, France.
Stefan OffermannsMax Planck Institute for Heart and Lung Research, Bad Nauheim, Germany.
Yuanyi FengDepartment of Neurology, Northwestern University, Chicago, IL, USA.
Amanda PatelInstitut de Pharmacologie Moléculaire et Cellulaire, LabEx ICST, UMR 7275 CNRS, Université de Nice Sophia Antipolis, Valbonne, France.
Eric HonoréInstitut de Pharmacologie Moléculaire et Cellulaire, LabEx ICST, UMR 7275 CNRS, Université de Nice Sophia Antipolis, Valbonne, France. honore@ipmc.cnrs.fr.
Fabrice DupratInstitut de Pharmacologie Moléculaire et Cellulaire, LabEx ICST, UMR 7275 CNRS, Université de Nice Sophia Antipolis, Valbonne, France.
Centre National de la Recherche Scientifique · FRLaboratoire d'Excellence Canaux Ioniques d'Intérêt Thérapeutique · FRInstitut de Pharmacologie Moléculaire et Cellulaire · FRMax Planck Institute for Heart and Lung Research · DENorthwestern University · USUniversité Paris Cité · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human mutations in the X-linked FLNA gene are associated with a remarkably diverse phenotype, including severe arterial morphological anomalies. However, the role for filamin A (FlnA) in vascular cells remains partially understood. We used a smooth muscle (sm)-specific conditional mouse model to delete FlnA at the adult stage, thus avoiding the developmental effects of the knock-out. Inactivation of smFlnA in adult mice significantly lowered blood pressure, together with a decrease in pulse pressure. However, both the aorta and carotid arteries showed a major outward hypertrophic remodeling, resistant to losartan, and normally occurring in hypertensive conditions. Notably, arterial compliance was significantly enhanced in the absence of smFlnA. Moreover, reactivity of thoracic aorta rings to a variety of vasoconstrictors was elevated, while basal contractility in response to KCl depolarization was reduced. Enhanced reactivity to the thromboxane A2 receptor agonist U46619 was fully reversed by the ROCK inhibitor Y27632. We discuss the possibility that a reduction in arterial stiffness upon smFlnA inactivation might cause a compensatory increase in conduit artery diameter for normalization of parietal tension, independently of the ROCK pathway. In conclusion, deletion of smFlnA in adult mice recapitulates the vascular phenotype of human bilateral periventricular nodular heterotopia, culminating in aortic dilatation.

Indexed as

AnimalsAortaBlood PressureCarotid ArteriesFilaminsHumansMaleMiceMuscle, Smooth, VascularPhenotypeVascular StiffnessVasoconstrictor AgentsFilaminsVasoconstrictor AgentsAortaBlood pressureCarotidContractilityFilamin AReactivityRemodelingStiffness

Identifiers

PMID27023351
OpenAlexW2312254308

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.