Evidence map›Paper›PMID 27252252›Full record

ArticlePhysiological reports2016

Limiting collagen turnover via collagenase-resistance attenuates right ventricular dysfunction and fibrosis in pulmonary arterial hypertension.

Mark J Golob, Zhijie Wang, Anthony J Prostrollo, Timothy A Hacker, Naomi C Chesler

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Physiological reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Review
  3. Molecular insights using spatial transcriptomics of the distal lung in congenital diaphragmatic hernia.American journal of physiology. Lung cellular and molecular physiology · 2023
    Article
  4. Review
  5. Article
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  14. Article
  15. Article
  16. Article
  17. Role of extracellular matrix in the pathogenesis of pulmonary arterial hypertension.American journal of physiology. Heart and circulatory physiology · 2018
    Review
  18. Multiscale structure-function relationships in right ventricular failure due to pressure overload.American journal of physiology. Heart and circulatory physiology · 2018
    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

5 authors at 2 institutions in 1 country.

Mark J GolobDepartment of Biomedical Engineering, University of Wisconsin-Madison College of Engineering, Madison, Wisconsin Materials Science Program, University of Wisconsin-Madison College of Engineering, Madison, Wisconsin.
Zhijie WangDepartment of Biomedical Engineering, University of Wisconsin-Madison College of Engineering, Madison, Wisconsin.
Anthony J ProstrolloDepartment of Biomedical Engineering, University of Wisconsin-Madison College of Engineering, Madison, Wisconsin.
Timothy A HackerDepartment of Medicine, Medical Science Center University of Wisconsin-Madison, Madison, Wisconsin.
Naomi C CheslerDepartment of Biomedical Engineering, University of Wisconsin-Madison College of Engineering, Madison, Wisconsin naomi.chesler@wisc.edu.
University of Wisconsin–Madison · USMadison Area Technical College · US

Funding

Vascular collagen accumulation & mechanical mechanisms in pulmonary hypertensionR01HL086939 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI CHESLER, NAOMI C · 2007 to 2016
$3.6M
NHLBI NIH HHS 1R01HL086939
6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a severe form of pulmonary hypertension in which right ventricular (RV) afterload is increased and death typically occurs due to decompensated RV hypertrophy and failure. Collagen accumulation has been implicated in pulmonary artery remodeling, but how it affects RV performance remains unclear. Here, we sought to identify the role of collagen turnover, defined as the balance between collagen synthesis and degradation, in RV structure and function in PAH To do so, we exposed mutant (Col1a1(R/R)) mice, in which collagen type I degradation is impaired such that collagen turnover is reduced, and wild-type (Col1a1(+/+)) littermates to 14 days of chronic hypoxia combined with SUGEN treatment (HySu) to recapitulate characteristics of clinical PAH RV structure and function were measured by echocardiography, RV catheterization, and histology. Despite comparable increases in RV systolic pressure (Col1a1(+/+): 46 ± 2 mmHg; Col1a1(R/R): 47 ± 3 mmHg), the impaired collagen degradation in Col1a1(R/R) mice resulted in no RV collagen accumulation, limited RV hypertrophy, and maintained right ventricular-pulmonary vascular coupling with HySu exposure. The preservation of cardiac function in the mutant mice indicates a beneficial role of limited collagen turnover via impaired degradation in RV remodeling in response to chronic pressure overload. Our results suggest novel treatments that reduce collagen turnover may offer a new therapeutic strategy for PAH patients.

Indexed as

AnimalsCollagenCollagenasesFibrosisHypertension, PulmonaryMiceMice, TransgenicVentricular Dysfunction, RightCollagenCollagenasesCardiac energeticseffective arterial elastancehypertrophypressure‐volume loop

Identifiers

PMID27252252
PMCPMC4908492
OpenAlexW2412492657

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.