Evidence map›Paper›PMID 31279666›Full record

ReviewTrends in endocrinology and metabolism: TEM2019

Interactive and Multifactorial Mechanisms of Calcific Vascular and Valvular Disease.

Linda L Demer, Yin Tintut

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Trends in endocrinology and metabolism: TEM, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.1field-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

15 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Skeleton-secreted PDGF-BB mediates arterial stiffening.The Journal of clinical investigation · 2021
    Article
  10. Article
  11. Role of Inflammation in Arterial Calcification.Korean circulation journal · 2021
    Review
  12. Article
  13. Advances in CT Techniques in Vascular Calcification.Frontiers in cardiovascular medicine · 2021
    Review
  14. Iron in Cardiovascular Disease: Challenges and Potentials.Frontiers in cardiovascular medicine · 2021
    Review
  15. 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

2 authors at 1 institution in 1 country.

Linda L DemerDepartment of Medicine, University of California at Los Angeles, Los Angeles, CA 90095-1679, USA; Department of Physiology, University of California at Los Angeles, Los Angeles, CA 90095-1751, USA; Department of Bioengineering, University of California at Los Angeles, Los Angeles, CA 90095-1600, USA. Electronic address: LDemer@mednet.ucla.edu.
Yin TintutDepartment of Medicine, University of California at Los Angeles, Los Angeles, CA 90095-1679, USA; Department of Physiology, University of California at Los Angeles, Los Angeles, CA 90095-1751, USA; Department of Orthopaedic Surgery, University of California at Los Angeles, Los Angeles, CA 90095, USA.
University of California, Los Angeles · US

Funding

Serotonin receptor contribution to inflammation-induced calcific aortic valve diseaseR01HL137647 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DEMER, LINDA L., TINTUT, YIN · 2019 to 2022
$1.6M
Mechanisms of intermittent parathyroid hormone effects on calcific aortic diseaseR01HL121019 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DEMER, LINDA L., TINTUT, YIN · 2015 to 2018
$1.5M
Does aging transform calcific vasculopathy into a plaque stabilizing process?R21AG061586 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DEMER, LINDA L., TINTUT, YIN · 2019 to 2020
$429k
NHLBI NIH HHS R01 HL121019NHLBI NIH HHS R01 HL137647NIA NIH HHS R21 AG061586
6 · The paper itself

Abstract

Calcific vascular and valvular disease (CVVD) is widespread and has major health consequences. Although coronary artery calcification has long been associated with hyperlipidemia and increased mortality, recent evidence suggests that its progression is increased in association with cholesterol-lowering HMG-CoA reductase inhibitors ('statins') and long-term, high-intensity exercise. A nationwide trial showed no cardiovascular benefit of vitamin D supplements. Controversy remains as to whether calcium deposits in plaque promote or prevent plaque rupture. CVVD appears to occur through mechanisms similar to those of intramembranous, endochondral, and osteophytic skeletal bone formation. New evidence implicates autotaxin, endothelial-mesenchymal transformation, and microRNA and long non-coding RNA (lncRNA) as novel regulatory factors. New therapeutic options are being developed.

Indexed as

AnimalsAtherosclerosisCardiovascular SystemHeart Valve DiseasesHumansHydroxymethylglutaryl-CoA Reductase InhibitorsVitamin DHydroxymethylglutaryl-CoA Reductase InhibitorsVitamin Datherosclerosisbonecalcificationcardiovascularvalvular disease

Identifiers

PMID31279666
PMCPMC6708492
OpenAlexW2955297526

What OpenQuestion holds

Texttitle and abstract
LicenceTDM
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.