Evidence map›Paper›PMID 27535662›Full record

ReviewCellular and molecular life sciences : CMLS2017

Vascular smooth muscle cells in Marfan syndrome aneurysm: the broken bricks in the aortic wall.

Gianluca L Perrucci, Erica Rurali, Aoife Gowran, Alessandro Pini, Carlo Antona, Roberto Chiesa, Giulio Pompilio, Patrizia Nigro

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2017. 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
6.0field-weighted citation impact, top 4% 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, 58 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Update in Biomolecular and Genetic Bases of Bicuspid Aortopathy.International journal of molecular sciences · 2021
    Review
  13. Review
  14. Vascular dysfunction and pathology: focus on mechanical forces.Vascular biology (Bristol, England) · 2021
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

8 authors at 4 institutions in 1 country.

Gianluca L PerrucciDepartment of Clinical Sciences and Community Health, University of Milan, Via Festa del Perdono 7, 20122, Milan, Italy.
Erica RuraliUnit of Vascular Biology and Regenerative Medicine, Centro Cardiologico Monzino-IRCCS, Via C. Parea 4, 20138, Milan, Italy.
Aoife GowranUnit of Vascular Biology and Regenerative Medicine, Centro Cardiologico Monzino-IRCCS, Via C. Parea 4, 20138, Milan, Italy.
Alessandro PiniDepartment of Cardiology, Marfan Clinic®, "Luigi Sacco" University of Milan, Via G.B. Grassi 74, 20157, Milan, Italy.
Carlo AntonaCardiovascular Surgery Department, "Luigi Sacco" University of Milan, Via G.B. Grassi 74, 20157, Milan, Italy.
Roberto ChiesaDepartment of Vascular Surgery, San Raffaele Scientific Institute Hospital, Vita-Salute University, Milan, Italy.
Giulio PompilioDepartment of Clinical Sciences and Community Health, University of Milan, Via Festa del Perdono 7, 20122, Milan, Italy. giulio.pompilio@ccfm.it.
Patrizia NigroUnit of Vascular Biology and Regenerative Medicine, Centro Cardiologico Monzino-IRCCS, Via C. Parea 4, 20138, Milan, Italy. patrizia.nigro@ccfm.it.
Centro Cardiologico Monzino · ITIstituti di Ricovero e Cura a Carattere Scientifico · ITUniversity of Milan · ITVita-Salute San Raffaele University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Marfan syndrome (MFS) is a connective tissue disorder with multiple organ manifestations. The genetic cause of this syndrome is the mutation of the FBN1 gene, encoding the extracellular matrix (ECM) protein fibrillin-1. This genetic alteration leads to the degeneration of microfibril structures and ECM integrity in the tunica media of the aorta. Indeed, thoracic aortic aneurysm and dissection represent the leading cause of death in MFS patients. To date, the most effective treatment option for this pathology is the surgical substitution of the damaged aorta. To highlight novel therapeutic targets, we review the molecular mechanisms related to MFS etiology in vascular smooth muscle cells, the foremost cellular type involved in MFS pathogenesis.

Indexed as

AneurysmAnimalsAortaHumansMarfan SyndromeMechanotransduction, CellularMuscle, Smooth, VascularMyocytes, Smooth MuscleAngiotensin IIMechanotrasductionMicroRNAMMPsTGF-beta

Identifiers

PMID27535662
PMCPMC11107581
OpenAlexW2516962876

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.