Evidence map›Paper›PMID 26009633›Full record

ArticleJournal of lipid research2015

PLTP activity inversely correlates with CAAD: effects of PON1 enzyme activity and genetic variants on PLTP activity.

Daniel Seung Kim, Amber A Burt, Jane E Ranchalis, Simona Vuletic, Tomas Vaisar, Wan-Fen Li, Elisabeth A Rosenthal, Weijiang Dong, Jason F Eintracht, Arno G Motulsky and 4 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
2.2field-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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.

  1. Pooled it
  2. Biomedicines · 2026
    Article
  3. Paraoxonase 1 and atherosclerosis.Frontiers in cardiovascular medicine · 2023
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. 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

14 authors at 3 institutions in 2 countries.

Daniel Seung KimDivision of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA Department of Biostatistics, University of Washington School of Public Health, Seattle, WA.
Amber A BurtDivision of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA.
Jane E RanchalisDivision of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA.
Simona VuleticNorthwest Lipid Metabolism and Diabetes Research Laboratories, Seattle, WA Division of Metabolism, Endocrinology, and Nutrition, Department of Medicine, University of Washington School of Medicine, Seattle, WA.
Tomas VaisarDivision of Metabolism, Endocrinology, and Nutrition, Department of Medicine, University of Washington School of Medicine, Seattle, WA.
Wan-Fen LiDivision of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA.
Elisabeth A RosenthalDivision of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA.
Weijiang DongNorthwest Lipid Metabolism and Diabetes Research Laboratories, Seattle, WA Division of Metabolism, Endocrinology, and Nutrition, Department of Medicine, University of Washington School of Medicine, Seattle, WA Department of Human Anatomy and Histology and Embryology, Xi'an Jiaotong University School of Medicine, Xi'an 710061, People's Republic of China.
Jason F EintrachtDepartment of General Medicine, Virginia Mason Medical Center, Seattle, WA.
Arno G MotulskyDivision of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA.
John D BrunzellDivision of Metabolism, Endocrinology, and Nutrition, Department of Medicine, University of Washington School of Medicine, Seattle, WA.
John J AlbersNorthwest Lipid Metabolism and Diabetes Research Laboratories, Seattle, WA Division of Metabolism, Endocrinology, and Nutrition, Department of Medicine, University of Washington School of Medicine, Seattle, WA.
Clement E FurlongDivision of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA.
Gail P JarvikDivision of Medical Genetics, Department of Medicine, University of Washington School of Medicine, Seattle, WA Department of Genome Sciences, University of Washington School of Medicine, Seattle, WA.
University of Washington Medical Center · USUniversity of Washington · USVirginia Mason Medical Center · US

Funding

WILDLIFE BIOMARKER APPLICATIONS TO REMEDIATION DECISION MAKINGP42ES004696 · NIEHS · UNIVERSITY OF WASHINGTON · PI GALLAGHER, EVAN P · 1987 to 2021
$51.2M
Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Tomas Vaisar · 1986 to 2026
$41.4M
Prediction and Progression of Carotid Artery DiseaseR01HL067406 · NHLBI · UNIVERSITY OF WASHINGTON · PI JARVIK, GAIL PAIRITZ · 2002 to 2009
$5.1M
Pharmacogenomics of serotonin-specific reuptake inhibitorsF31MH101905 · NIMH · UNIVERSITY OF WASHINGTON · PI KIM, DANIEL SEUNG · 2013 to 2014
$70k
NHLBI NIH HHS R01 HL067406NHLBI NIH HHS R01 HL67406NIDDK NIH HHS P30 DK017047NIEHS NIH HHS P42 ES004696NIMH NIH HHS 1F31MH101905-01NIMH NIH HHS F31 MH101905
6 · The paper itself

Abstract

Recent studies have failed to demonstrate a causal cardioprotective effect of HDL cholesterol levels, shifting focus to the functional aspects of HDL. Phospholipid transfer protein (PLTP) is an HDL-associated protein involved in reverse cholesterol transport. This study sought to determine the genetic and nongenetic predictors of plasma PLTP activity (PLTPa), and separately, to determine whether PLTPa predicted carotid artery disease (CAAD). PLTPa was measured in 1,115 European ancestry participants from a case-control study of CAAD. A multivariate logistic regression model was used to elucidate the relationship between PLTPa and CAAD. Separately, a stepwise linear regression determined the nongenetic clinical and laboratory characteristics that best predicted PLTPa. A final stepwise regression considering both nongenetic and genetic variables identified the combination of covariates that explained maximal PLTPa variance. PLTPa was significantly associated with CAAD (7.90 × 10(-9)), with a 9% decrease in odds of CAAD per 1 unit increase in PLTPa (odds ratio = 0.91). Triglyceride levels (P = 0.0042), diabetes (P = 7.28 × 10(-5)), paraoxonase 1 (PON1) activity (P = 0.019), statin use (P = 0.026), PLTP SNP rs4810479 (P = 6.38 × 10(-7)), and PCIF1 SNP rs181914932 (P = 0.041) were all significantly associated with PLTPa. PLTPa is significantly inversely correlated with CAAD. Furthermore, we report a novel association between PLTPa and PON1 activity, a known predictor of CAAD.

Indexed as

Polymorphism, Single NucleotideAgedAryldialkylphosphataseCarotid Artery DiseasesCase-Control StudiesFemaleHumansLipidsMaleMultivariate AnalysisPhospholipid Transfer ProteinsAryldialkylphosphataseLipidsPhospholipid Transfer ProteinsPON1 protein, humancoronary artery diseaseparaoxonase 1phospholipid transfer protein

Identifiers

PMID26009633
PMCPMC4479339
OpenAlexW2286033299

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.