Evidence map›Paper›PMID 25535288›Full record

ArticleJournal of lipid research2015

Influence of physiological changes in endogenous estrogen on circulating PCSK9 and LDL cholesterol.

Moumita Ghosh, Cecilia Gälman, Mats Rudling, Bo Angelin

Erratum issuedOpen 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. An erratum has been issued. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 5% 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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 114 citations in OpenAlex.

  1. Pooled it
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  9. Exploring sex bias in cardiometabolic diseases.Lipids in health and disease · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 1 country.

Moumita GhoshMetabolism Unit, Department of Endocrinology, Metabolism, and Diabetes, Karolinska Institutet at Karolinska University Hospital Huddinge, C2-94, S-141 86 Stockholm, Sweden Molecular Nutrition Unit, Center for Innovative Medicine, Karolinska Institutet at Karolinska University Hospital Huddinge, C2-94, S-141 86 Stockholm, Sweden Karolinska Institutet/AstraZeneca Integrated CardioMetabolic Center, Department of Medicine, Karolinska Institutet at Karolinska University Hospital Huddinge, C2-94, S-141 86 Stockholm, Sweden.
Cecilia GälmanMetabolism Unit, Department of Endocrinology, Metabolism, and Diabetes, Karolinska Institutet at Karolinska University Hospital Huddinge, C2-94, S-141 86 Stockholm, Sweden Molecular Nutrition Unit, Center for Innovative Medicine, Karolinska Institutet at Karolinska University Hospital Huddinge, C2-94, S-141 86 Stockholm, Sweden.
Mats RudlingMetabolism Unit, Department of Endocrinology, Metabolism, and Diabetes, Karolinska Institutet at Karolinska University Hospital Huddinge, C2-94, S-141 86 Stockholm, Sweden Molecular Nutrition Unit, Center for Innovative Medicine, Karolinska Institutet at Karolinska University Hospital Huddinge, C2-94, S-141 86 Stockholm, Sweden Karolinska Institutet/AstraZeneca Integrated CardioMetabolic Center, Department of Medicine, Karolinska Institutet at Karolinska University Hospital Huddinge, C2-94, S-141 86 Stockholm, Sweden.
Bo AngelinMetabolism Unit, Department of Endocrinology, Metabolism, and Diabetes, Karolinska Institutet at Karolinska University Hospital Huddinge, C2-94, S-141 86 Stockholm, Sweden Molecular Nutrition Unit, Center for Innovative Medicine, Karolinska Institutet at Karolinska University Hospital Huddinge, C2-94, S-141 86 Stockholm, Sweden Karolinska Institutet/AstraZeneca Integrated CardioMetabolic Center, Department of Medicine, Karolinska Institutet at Karolinska University Hospital Huddinge, C2-94, S-141 86 Stockholm, Sweden.
AstraZeneca (Sweden) · SEKarolinska Institutet · SEKarolinska University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pharmacologically increased estrogen levels have been shown to lower hepatic and plasma proprotein convertase subtilisin/kexin type 9 (PCSK9) levels in animals and humans. We hypothesized that physiological changes in estrogen levels influence circulating PCSK9, thereby contributing to the known wide inter-individual variation in its plasma levels, as well as to the established increase in LDL cholesterol (LDL-C) with normal aging. Circulating PCSK9, estradiol, and other metabolic factors were determined in fasting samples from 206 female and 189 male healthy volunteers (age 20-85 years), The mean levels of PCSK9 were 10% higher in females than in males (P < 0.05). PCSK9 levels were 22% higher in postmenopausal than in premenopausal (P < 0.001) females. Within the group of premenopausal females, circulating PCSK9 correlated inversely to estrogen levels, and PCSK9 was higher (305 ng/ml) in the follicular phase than in the ovulatory (234 ng/ml) or the luteal (252 ng/ml) phases (P < 0.05). Changes in endogenous estrogen levels during the menstrual cycle likely contribute to the broad inter-individual variation in PCSK9 and LDL-C in normal females. PCSK9 levels increase in females after menopause but not in men during this phase in life. This likely contributes to why LDL-C in women increases in this period.

Indexed as

AdultAgedAged, 80 and overCholesterol, LDLEstrogensFemaleHumansMaleMenstrual CycleMiddle AgedProprotein Convertase 9Proprotein ConvertasesSerine EndopeptidasesSex FactorsYoung AdultCholesterol, LDLEstrogensPCSK9 protein, humanProprotein Convertase 9Proprotein ConvertasesSerine Endopeptidaseslow density lipoprotein cholesterolmenopausemenstruation cycleproprotein convertase subtilisin/kexin type 9

Identifiers

PMID25535288
PMCPMC4306699
OpenAlexW2037547169

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.