Evidence map›Paper›PMID 35024504›Full record

ArticleJACC. Basic to translational science2021

Abnormal Flow Conditions Promote Endocardial Fibroelastosis Via Endothelial-to-Mesenchymal Transition, Which Is Responsive to Losartan Treatment.

Nicholas A Oh, Xuechong Hong, Ilias P Doulamis, Elamaran Meibalan, Teresa Peiseler, Juan Melero-Martin, Guillermo García-Cardeña, Pedro J Del Nido, Ingeborg Friehs

Open access · goldAbstract read
In one paragraph

Article in JACC. Basic to translational science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Fibroelastic Remodelling of the Endocardium on the Right Side of the Heart: Endothelial-to-Mesenchymal Transition in Pulmonary Atresia With Intact Ventricular Septum.European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery · 2026
    Article
  7. Shear stress-induced CaBiological research · 2026
    Article
  8. Review
  9. Article
  10. Article
  11. Eliminating left ventricular outlet stenosis lowers the risk for endocardial fibroelastosis recurrence†.European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery · 2025
    Article
  12. Observational
  13. Review
  14. Endocardium in Hypoplastic Left Heart Syndrome: Implications from In Vitro Study.Journal of cardiovascular development and disease · 2022
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. 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

9 authors at 3 institutions in 1 country.

Nicholas A OhDepartment of Cardiac Surgery, Boston Children's Hospital, Boston, Massachusetts, USA.
Xuechong HongDepartment of Cardiac Surgery, Boston Children's Hospital, Boston, Massachusetts, USA.
Ilias P DoulamisDepartment of Cardiac Surgery, Boston Children's Hospital, Boston, Massachusetts, USA.
Elamaran MeibalanLaboratory for Systems Mechanobiology, Center for Excellence in Vascular Biology, Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts, USA.
Teresa PeiselerDepartment of Cardiac Surgery, Boston Children's Hospital, Boston, Massachusetts, USA.
Juan Melero-MartinDepartment of Cardiac Surgery, Boston Children's Hospital, Boston, Massachusetts, USA.
Guillermo García-CardeñaLaboratory for Systems Mechanobiology, Center for Excellence in Vascular Biology, Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts, USA.
Pedro J Del NidoDepartment of Cardiac Surgery, Boston Children's Hospital, Boston, Massachusetts, USA.
Ingeborg FriehsDepartment of Cardiac Surgery, Boston Children's Hospital, Boston, Massachusetts, USA.
Boston Children's Hospital · USBrigham and Women's Hospital · USCleveland Clinic · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endocardial fibroelastosis (EFE) is defined by fibrotic tissue on the endocardium and forms partly through aberrant endothelial-to-mesenchymal transition. However, the pathologic triggers are still unknown. In this study, we showed that abnormal flow induces EFE partly through endothelial-to-mesenchymal transition in a rodent model, and that losartan can abrogate EFE development. Furthermore, we translated our findings to human endocardial endothelial cells, and showed that laminar flow promotes the suppression of genes associated with mesenchymal differentiation. These findings emphasize the role of flow in promoting EFE in endocardial endothelial cells and provide a novel potential therapy to treat this highly morbid condition.

Indexed as

AR, aortic regurgitationcongenital heart diseaseEFE, endocardial fibroelastosisendocardial endothelial cellsendocardial fibroelastosisEndoMT, endothelial-to-mesenchymal transitionendothelial-to-mesenchymal transitionGO, gene ontologyHLHS, hypoplastic left heart syndromeHUEEC, human endocardial endothelial cellsHUVEC, human umbilical vein endothelial cellsLSS, laminar shear stressLV, left ventriclewall shear stressα-SMA, alpha-smooth muscle actin

Identifiers

PMID35024504
PMCPMC8733675
OpenAlexW3160546402

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.