Evidence map›Paper›PMID 29594151›Full record

ArticleFrontiers in cardiovascular medicine2018

Advances in Pathophysiology of Calcific Aortic Valve Disease Propose Novel Molecular Therapeutic Targets.

Alexia Hulin, Alexandre Hego, Patrizio Lancellotti, Cécile Oury

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cardiovascular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
5.3field-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

34 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Glycemic control after aortic valve replacement: A retrospective study.International journal of cardiology. Heart & vasculature · 2025
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Aortic stenosis: a review on acquired pathogenesis and ominous combination with diabetes mellitus.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2023
    Review
  12. Article
  13. Mechanical injury accentuates lipid deposition in ApoEFrontiers in cardiovascular medicine · 2023
    Article
  14. Article
  15. Article
  16. Review
  17. Monocytes augment inflammatory responses in human aortic valve interstitial cells via βInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Article
  18. Article
  19. Review
  20. Observational
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

4 authors at 1 institution in 1 country.

Alexia HulinGIGA Cardiovascular Sciences, Laboratory of Thrombosis and Hemostasis and Valvular Heart Disease, University of Liège, CHU Sart Tilman, Liège, Belgium.
Alexandre HegoGIGA Cardiovascular Sciences, Laboratory of Thrombosis and Hemostasis and Valvular Heart Disease, University of Liège, CHU Sart Tilman, Liège, Belgium.
Patrizio LancellottiGIGA Cardiovascular Sciences, Laboratory of Thrombosis and Hemostasis and Valvular Heart Disease, University of Liège, CHU Sart Tilman, Liège, Belgium.
Cécile OuryGIGA Cardiovascular Sciences, Laboratory of Thrombosis and Hemostasis and Valvular Heart Disease, University of Liège, CHU Sart Tilman, Liège, Belgium.
University of Liège · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calcific Aortic Valve Disease (CAVD) is the most common heart valve disease and its incidence is expected to rise with aging population. No medical treatment so far has shown slowing progression of CAVD progression. Surgery remains to this day the only way to treat it. Effective drug therapy can only be achieved through a better insight into the pathogenic mechanisms underlying CAVD. The cellular and molecular events leading to leaflets calcification are complex. Upon endothelium cell damage, oxidized LDLs trigger a proinflammatory response disrupting healthy cross-talk between valve endothelial and interstitial cells. Therefore, valve interstitial cells transform into osteoblasts and mineralize the leaflets. Studies have investigated signaling pathways driving and connecting lipid metabolism, inflammation and osteogenesis. This review draws a summary of the recent advances and discusses their exploitation as promising therapeutic targets to treat CAVD and reduce valve replacement.

Indexed as

calcific aortic valve diseasecalcificationinflammationlipidsoxidative stresssignal transduction

Identifiers

PMID29594151
PMCPMC5862098
OpenAlexW2790345314

What Socratic 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 Socratic graph.