Evidence map›Paper›PMID 29369739›Full record

ArticleJournal of applied physiology (Bethesda, Md. : 1985)2018

Organ-level right ventricular dysfunction with preserved Frank-Starling mechanism in a mouse model of pulmonary arterial hypertension.

Zhijie Wang, Jitandrakumar R Patel, David A Schreier, Timothy A Hacker, Richard L Moss, Naomi C Chesler

Open access · bronzeAbstract read
In one paragraph

Article in Journal of applied physiology (Bethesda, Md. : 1985), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. [Research progress of right ventricular strain imaging evaluation technology in pulmonary arterial hypertension].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2024
    Review
  6. Sex-dependent remodeling of right ventricular function in a rat model of pulmonary arterial hypertension.American journal of physiology. Heart and circulatory physiology · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Sex differences in right ventricular adaptation to pressure overload in a rat model.Journal of applied physiology (Bethesda, Md. : 1985) · 2022
    Article
  11. Review
  12. Article
  13. Review
  14. Estrogen receptor-α prevents right ventricular diastolic dysfunction and fibrosis in female rats.American journal of physiology. Heart and circulatory physiology · 2020
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Multiscale structure-function relationships in right ventricular failure due to pressure overload.American journal of physiology. Heart and circulatory physiology · 2018
    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

6 authors at 1 institution in 1 country.

Zhijie WangDepartment of Biomedical Engineering, University of Wisconsin-Madison , Madison, Wisconsin.ORCID 0000-0001-9551-516X
Jitandrakumar R PatelDepartment of Cell and Regenerative Biology, University of Wisconsin-Madison , Madison, Wisconsin.
David A SchreierDepartment of Biomedical Engineering, University of Wisconsin-Madison , Madison, Wisconsin.
Timothy A HackerDepartment of Medicine, University of Wisconsin-Madison , Madison, Wisconsin.
Richard L MossDepartment of Cell and Regenerative Biology, University of Wisconsin-Madison , Madison, Wisconsin.
Naomi C CheslerDepartment of Biomedical Engineering, University of Wisconsin-Madison , Madison, Wisconsin.
University of Wisconsin–Madison · US

Funding

Vascular collagen accumulation & mechanical mechanisms in pulmonary hypertensionR01HL086939 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI CHESLER, NAOMI C · 2007 to 2016
$3.6M
Right Heart-Pulmonary Vascular Interactions in Bronchopulmonary DysplasiaR01HL115061 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI ELDRIDGE, MARLOWE · 2012 to 2016
$3.2M
NHLBI NIH HHS R01 HL115061
6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a rapidly fatal disease in which mortality is due to right ventricular (RV) failure. It is unclear whether RV dysfunction initiates at the organ level or the subcellular level or both. We hypothesized that chronic pressure overload-induced RV dysfunction begins at the organ level with preserved Frank-Starling mechanism in myocytes. To test this hypothesis, we induced PAH with Sugen + hypoxia (HySu) in mice and measured RV whole organ and subcellular functional changes by in vivo pressure-volume measurements and in vitro trabeculae length-tension measurements, respectively, at multiple time points for up to 56 days. We observed progressive changes in RV function at the organ level: in contrast to early PAH (14-day HySu), in late PAH (56-day HySu) ejection fraction and ventricular-vascular coupling were decreased. At the subcellular level, direct measurements of myofilament contraction showed that RV contractile force was similarly increased at any stage of PAH development. Moreover, cross-bridge kinetics were not changed and length dependence of force development (Frank-Starling relation) were not different from baseline in any PAH group. Histological examinations confirmed increased cardiomyocyte cross-sectional area and decreased von Willebrand factor expression in RVs with PAH. In summary, RV dysfunction developed at the organ level with preserved Frank-Starling mechanism in myofilaments, and these results provide novel insight into the development of RV dysfunction, which is critical to understanding the mechanisms of RV failure. NEW & NOTEWORTHY A multiscale investigation of pulmonary artery pressure overload in mice showed time-dependent organ-level right ventricular (RV) dysfunction with preserved Frank-Starling relations in myofilaments. Our findings provide novel insight into the development of RV dysfunction, which is critical to understanding mechanisms of RV failure.

Indexed as

AnimalsDisease Models, AnimalHeart FailureHeart VentriclesHypertension, PulmonaryHypoxiaMaleMiceMice, Inbred C57BLMyocardial ContractionMyocytes, CardiacPulmonary ArteryVentricular Dysfunction, RightVentricular Function, Righthypertrophymyocyte morphologyright heart failureskinned trabeculaeventricular-vascular coupling

Identifiers

PMID29369739
PMCPMC6008075
OpenAlexW2785228604

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.