Evidence map›Paper›PMID 9062358›Full record

ArticleThe Journal of clinical investigation1997

Increased cellular expression of matrix proteins that regulate mineralization is associated with calcification of native human and porcine xenograft bioprosthetic heart valves.

S S Srivatsa, P J Harrity, P B Maercklein, L Kleppe, J Veinot, W D Edwards, C M Johnson, L A Fitzpatrick

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
5.4field-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

35 citing papers in PubMed, 171 citations in OpenAlex.

  1. Review
  2. Article
  3. Calcific Aortic Valve Stenosis with Aging and Current Development in its Pathophysiology.The International journal of angiology : official publication of the International College of Angiology, Inc · 2022
    Article
  4. Article
  5. Bone Health in Patients with Dyslipidemias: An Underestimated Aspect.International journal of molecular sciences · 2022
    Review
  6. Review
  7. Role of Runx2 in Calcific Aortic Valve Disease in Mouse Models.Frontiers in cardiovascular medicine · 2021
    Article
  8. Review
  9. Degeneration of Bioprosthetic Heart Valves: Update 2020.Journal of the American Heart Association · 2020
    Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Pathophysiology of valvular heart disease.Experimental and therapeutic medicine · 2016
    Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review
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 1 institution in 1 country.

S S SrivatsaDepartment of Internal Medicine, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55905, USA.
P J Harrity
P B Maercklein
L Kleppe
J Veinot
W D Edwards
C M Johnson
L A Fitzpatrick
Mayo Clinic · US

Funding

ESTROGEN STATUS AND THE FUNCTION OF CORONARY ARTERIESR01HL051736 · NHLBI · MAYO CLINIC COLL OF MEDICINE, ROCHESTER · PI MILLER, VIRGINIA M · 1994 to 2002
$1.0M
NHLBI NIH HHS NHLB 51736
6 · The paper itself

Abstract

Dystrophic mineralization remains the leading cause of stenotic or regurgitant failure in native human and porcine bioprosthetic heart valves. We hypothesized that cellular expression of noncollagenous matrix proteins (osteopontin, osteocalcin, and osteonectin) that regulate skeletal mineralization may orchestrate valvular calcification. Porcine bioprosthetic heart valves and native human heart valves obtained during replacement surgery were analyzed for cells, matrix proteins that regulate mineralization, and vessels. Cell accumulation and calcification were correlated for both valve types (rho = 0.75, P = 0.01, native; rho = 0.42, P = 0.08, bioprosthetic). Osteopontin expression correlated with cell accumulation (rho = 0.58, P = 0.04) and calcification (rho = 0.52, P = 0.06) for bioprosthetic valves. Osteocalcin expression correlated with calcification (rho = 0.77, P = 0.04) and cell accumulation (rho = 0.69, P = 0.07) in native valves. Comparisons of calcified versus noncalcified native and bioprosthetic valves for averaged total matrix protein mRNA signal score revealed increased noncollagenous proteins mRNA levels in calcified valves (P = 0.07, group I vs. group II; P = 0.02, group III vs. group IV). When stratified according to positive versus negative mRNA signal status, both calcified bioprosthetic valves (P = 0.03) and calcified native valves (P = 0.01) were significantly more positive for noncollagenous proteins mRNA than their noncalcified counterparts. Local cell-associated expression of proteins regulating mineralization suggests a highly coordinated mechanism of bioprosthetic and native valve calcification analogous to physiologic bone mineralization. Modulation of cellular infiltration or cellular expression of matrix proteins that regulate mineralization, may offer an effective therapeutic approach to the prevention of valve failure secondary to calcification.

Indexed as

AgedAnimalsAntigens, CDAntigens, Differentiation, MyelomonocyticBioprosthesisCalcification, PhysiologicCalcinosisCardiomyopathiesCD68 MoleculeCell MovementDNA ProbesGene LibraryHeart Valve ProsthesisHeart ValvesHumansImmunohistochemistryAntigens, CDAntigens, Differentiation, MyelomonocyticCD68 antigen, humanCD68 MoleculeDNA ProbesOsteocalcinOsteonectinOsteopontinRNA, MessengerSialoglycoproteinsSPP1 protein, human

Identifiers

PMID9062358
PMCPMC507908
OpenAlexW1983529229

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.