Evidence map›Paper›PMID 28003526›Full record

ArticleJournal of the Royal Society, Interface2016

Differential cell-matrix responses in hypoxia-stimulated aortic versus mitral valves.

Matthew C Sapp, Varun K Krishnamurthy, Daniel S Puperi, Saheba Bhatnagar, Gabrielle Fatora, Neelesh Mutyala, K Jane Grande-Allen

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the Royal Society, Interface, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-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

13 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Role of hypoxia inducible factor HIF-1Global cardiology science & practice · 2023
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Chondromodulin-1 in health, osteoarthritis, cancer, and heart disease.Cellular and molecular life sciences : CMLS · 2019
    Review
  12. Article
  13. 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

7 authors at 2 institutions in 1 country.

Matthew C SappDepartment of Bioengineering, Rice University, Houston, TX 77005, USA.
Varun K KrishnamurthyDepartment of Bioengineering, Rice University, Houston, TX 77005, USA.
Daniel S PuperiDepartment of Bioengineering, Rice University, Houston, TX 77005, USA.
Saheba BhatnagarDepartment of Bioengineering, Rice University, Houston, TX 77005, USA.
Gabrielle FatoraDepartment of Bioengineering, Rice University, Houston, TX 77005, USA.
Neelesh MutyalaDepartment of Bioengineering, Rice University, Houston, TX 77005, USA.
K Jane Grande-AllenDepartment of Bioengineering, Rice University, Houston, TX 77005, USA grande@rice.edu.
Google (United States) · USRice University · US

Funding

American Heart Association-American Stroke Association 13POST16350003
6 · The paper itself

Abstract

Tissue oxygenation often plays a significant role in disease and is an essential design consideration for tissue engineering. Here, oxygen diffusion profiles of porcine aortic and mitral valve leaflets were determined using an oxygen diffusion chamber in conjunction with computational models. Results from these studies revealed the differences between aortic and mitral valve leaflet diffusion profiles and suggested that diffusion alone was insufficient for normal oxygen delivery in mitral valves. During fibrotic valve disease, leaflet thickening due to abnormal extracellular matrix is likely to reduce regional oxygen availability. To assess the impact of low oxygen levels on valve behaviour, whole leaflet organ cultures were created to induce leaflet hypoxia. These studies revealed a loss of layer stratification and elevated levels of hypoxia inducible factor 1-alpha in both aortic and mitral valve hypoxic groups. Mitral valves also exhibited altered expression of angiogenic factors in response to low oxygen environments when compared with normoxic groups. Hypoxia affected aortic and mitral valves differently, and mitral valves appeared to show a stenotic, rheumatic phenotype accompanied by significant cell death. These results indicate that hypoxia could be a factor in mid to late valve disease progression, especially with the reduction in chondromodulin-1 expression shown by hypoxic mitral valves.

Indexed as

AnimalsAortaExtracellular MatrixFibrosisHeart Valve DiseasesMitral ValveMyocardial IschemiaSwineangiogenesiscalcificationextracellular matrixheart valveoxygen diffusion

Identifiers

PMID28003526
PMCPMC5221519
OpenAlexW2562420389

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.