Evidence map›Paper›PMID 30533416›Full record

ReviewFrontiers in cardiovascular medicine2018

Lipoproteins in Cardiovascular Calcification: Potential Targets and Challenges.

Yin Tintut, Jeffrey J Hsu, Linda L Demer

Open access · goldAbstract readReview
In one paragraph

Review 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 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 13% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Oxidized Phospholipids and Calcific Aortic Valvular Disease.Journal of the American College of Cardiology · 2024
    Pooled it
  2. Observational
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
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  15. Article
  16. Article
  17. Article
  18. Skeleton-secreted PDGF-BB mediates arterial stiffening.The Journal of clinical investigation · 2021
    Article
  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

3 authors at 1 institution in 1 country.

Yin TintutDepartment of Medicine, University of California, Los Angeles, Los Angeles, CA, United States.
Jeffrey J HsuDepartment of Medicine, University of California, Los Angeles, Los Angeles, CA, United States.
Linda L DemerDepartment of Medicine, University of California, Los Angeles, Los Angeles, CA, United States.
University of California, Los Angeles · US

Funding

CARDIOVASCULAR SCIENTIST TRAINING PROGRAMT32HL007895 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SHIVKUMAR, KALYANAM, WATSON, KAROL E · 1998 to 2023
$9.2M
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
NHLBI NIH HHS R01 HL121019NHLBI NIH HHS T32 HL007895
6 · The paper itself

Abstract

Previously considered a degenerative process, cardiovascular calcification is now established as an active process that is regulated in several ways by lipids, phospholipids, and lipoproteins. These compounds serve many of the same functions in vascular and valvular calcification as they do in skeletal bone calcification. Hyperlipidemia leads to accumulation of lipoproteins in the subendothelial space of cardiovascular tissues, which leads to formation of mildly oxidized phospholipids, which are known bioactive factors in vascular cell calcification. One lipoprotein of particular interest is Lp(a), which showed genome-wide significance for the presence of aortic valve calcification and stenosis. It carries an important enzyme, autotaxin, which produces lysophosphatidic acid (LPA), and thus has a key role in inflammation among other functions. Matrix vesicles, extruded from the plasma membrane of cells, are the sites of initiation of mineral formation. Phosphatidylserine, a phospholipid in the membranes of matrix vesicles, is believed to complex with calcium and phosphate ions, creating a nidus for hydroxyapatite crystal formation in cardiovascular as well as in skeletal bone mineralization. This review focuses on the contributions of lipids, phospholipids, lipoproteins, and autotaxin in cardiovascular calcification, and discusses possible therapeutic targets.

Indexed as

autotaxincalcificationlipoproteinsLp(a)osteogenesis

Identifiers

PMID30533416
PMCPMC6265366
OpenAlexW2901552482

What OpenQuestion 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 OpenQuestion graph.