Evidence map›Paper›PMID 23833294›Full record

ReviewCirculation research2013

Molecular and cellular aspects of calcific aortic valve disease.

Dwight A Towler

Open access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers.

0numbers the graph read from it
0cells of the map it votes in
107citing papers in PubMed
8.9field-weighted citation impact, top 2% 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

107 citing papers in PubMed, 188 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Observational
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. The Role of miR-138 in Cardiovascular Diseases.BioMed research international · 2025
    Review
  12. Progress on long non-coding RNAs in calcific aortic valve disease.Frontiers in cardiovascular medicine · 2025
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Endovascular Drug Delivery.Life (Basel, Switzerland) · 2024
    Review
  18. Article
  19. Article
  20. Article

47 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Dwight A TowlerDiabetes and Obesity Research Center, Sanford-Burnham Medical Research Institute at Lake Nona, Orlando, FL 32827, USA. dtowler@sanfordburnham.org
Translational Research Institute for Metabolism and Diabetes · US

Funding

OSTEOGENIC REGULATION OF VASCULAR CALCIFICATIONR01HL069229 · NHLBI · WASHINGTON UNIVERSITY · PI TOWLER, DWIGHT A. · 2001 to 2022
$7.9M
Apoptosis and defective repair in COPDR01HL088138 · NHLBI · NATIONAL JEWISH HEALTH · PI HENSON, PETER M · 2008 to 2012
$3.5M
MSX2-WNT SIGNALING IN CARDIOVASCULAR CALCIFICATIONR01HL081138 · NHLBI · WASHINGTON UNIVERSITY · PI TOWLER, DWIGHT A. · 2005 to 2013
$3.4M
Endocrine Regulation of Calcific Aortic Valve Sclerosis: PTH/PTHRP Receptor SignaR01HL114806 · NHLBI · WASHINGTON UNIVERSITY · PI TOWLER, DWIGHT A. · 2012 to 2016
$2.1M
TNF-ALPHA AND BMP2-WNT SIGNALING IN DIABETIC VASCULAR DISEASER01HL088651 · NHLBI · WASHINGTON UNIVERSITY · PI TOWLER, DWIGHT A. · 2008 to 2012
$1.9M
NHLBI NIH HHS HL069229NHLBI NIH HHS HL088138NHLBI NIH HHS HL088651NHLBI NIH HHS HL114806NHLBI NIH HHS R01 HL069229NHLBI NIH HHS R01 HL081138NHLBI NIH HHS R01 HL088138NHLBI NIH HHS R01 HL088651NHLBI NIH HHS R01 HL114806
6 · The paper itself

Abstract

Calcific aortic valve disease (CAVD) increasingly afflicts our aging population. One third of our elderly have echocardiographic or radiological evidence of calcific aortic valve sclerosis, an early and subclinical form of CAVD. Age, sex, tobacco use, hypercholesterolemia, hypertension, and type II diabetes mellitus all contribute to the risk of disease that has worldwide distribution. On progression to its most severe form, calcific aortic stenosis, CAVD becomes debilitating and devastating, and 2% of individuals >60 years are affected by calcific aortic stenosis to the extent that surgical intervention is required. No effective pharmacotherapies exist for treating those at risk for clinical progression. It is becoming increasingly apparent that a diverse spectrum of cellular and molecular mechanisms converge to regulate valvular calcium load; this is evidenced not only in histopathologic heterogeneity of CAVD, but also from the multiplicity of cell types that can participate in valve biomineralization. In this review, we highlight our current understanding of CAVD disease biology, emphasizing molecular and cellular aspects of its regulation. We end by pointing to important biological and clinical questions that must be answered to enable sophisticated disease staging and the development of new strategies to treat CAVD medically.

Indexed as

AnimalsAortic ValveBicuspid Aortic Valve DiseaseCalcinosisCardiomyopathiesHeart Defects, CongenitalHeart Valve DiseasesHumansMyocytes, Cardiacaortic valve, calcification ofvascular calcificationvascular senescence

Identifiers

PMID23833294
PMCPMC4057916
OpenAlexW2127565475

What OpenQuestion holds

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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.