Evidence map›Paper›PMID 31599473›Full record

ArticleJournal of pineal research2020

Disruption of circadian rhythm by alternating light-dark cycles aggravates atherosclerosis development in APOE*3-Leiden.CETP mice.

Maaike Schilperoort, Rosa van den Berg, Laura A Bosmans, Bram W van Os, Martijn E T Dollé, Noortje A M Smits, Teun Guichelaar, Debbie van Baarle, Lotte Koemans, Jimmy F P Berbée and 11 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of pineal research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 74 citations in OpenAlex.

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  12. Acrolein-triggered atherosclerosisJournal of biomedical research · 2024
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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

21 authors at 4 institutions in 3 countries.

Maaike SchilperoortDivision of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands.ORCID https://orcid.org/0000-0002-8597-7675
Rosa van den BergDivision of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands.ORCID https://orcid.org/0000-0001-7677-1336
Laura A BosmansDepartment of Medical Biochemistry, Amsterdam Cardiovascular Sciences, Amsterdam University Medical Centre, University of Amsterdam, Amsterdam, The Netherlands.
Bram W van OsDepartment of Medical Biochemistry, Amsterdam Cardiovascular Sciences, Amsterdam University Medical Centre, University of Amsterdam, Amsterdam, The Netherlands.
Martijn E T DolléCentre for Health Protection, National Institute for Public Health and the Environment, Bilthoven, The Netherlands.
Noortje A M SmitsCenter for Infectious Disease Control, National Institute for Public Health and the Environment, Bilthoven, The Netherlands.
Teun GuichelaarCenter for Infectious Disease Control, National Institute for Public Health and the Environment, Bilthoven, The Netherlands.ORCID https://orcid.org/0000-0002-5112-8923
Debbie van BaarleCenter for Infectious Disease Control, National Institute for Public Health and the Environment, Bilthoven, The Netherlands.
Lotte KoemansDivision of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands.
Jimmy F P BerbéeDivision of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands.ORCID https://orcid.org/0000-0001-9133-3297
Tom DeboerDepartment of Molecular Cell Biology, Laboratory for Neurophysiology, Leiden University Medical Center, Leiden, The Netherlands.ORCID https://orcid.org/0000-0002-6402-6248
Johanna H MeijerDepartment of Molecular Cell Biology, Laboratory for Neurophysiology, Leiden University Medical Center, Leiden, The Netherlands.ORCID https://orcid.org/0000-0001-6619-5312
Margreet R de VriesEinthoven Laboratory for Experimental Vascular Medicine, Leiden, The Netherlands.ORCID https://orcid.org/0000-0002-3648-9130
Dianne VreekenEinthoven Laboratory for Experimental Vascular Medicine, Leiden, The Netherlands.
Janine M van GilsEinthoven Laboratory for Experimental Vascular Medicine, Leiden, The Netherlands.ORCID https://orcid.org/0000-0003-2429-7462
Ko Willems van DijkDivision of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands.ORCID https://orcid.org/0000-0002-2172-7394
Linda W M van KerkhofCentre for Health Protection, National Institute for Public Health and the Environment, Bilthoven, The Netherlands.ORCID https://orcid.org/0000-0001-5742-2659
Esther LutgensDepartment of Medical Biochemistry, Amsterdam Cardiovascular Sciences, Amsterdam University Medical Centre, University of Amsterdam, Amsterdam, The Netherlands.ORCID https://orcid.org/0000-0002-2609-5744
Nienke R BiermaszDivision of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands.ORCID https://orcid.org/0000-0001-5817-3594
Patrick C N RensenDivision of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands.ORCID https://orcid.org/0000-0002-8455-4988
Sander KooijmanDivision of Endocrinology, Department of Medicine, Leiden University Medical Center, Leiden, The Netherlands.ORCID https://orcid.org/0000-0002-0014-5571
Leiden University Medical Center · NLNational Institute for Public Health and the Environment · NLAmsterdam University Medical Centers · NLThe University of Texas Health Science Center at San Antonio · US

Funding

ENERGISE CVON2014-02Hartstichting 2013T127Hartstichting 2017T016Leids Universitair Medisch CentrumNederlandse Organisatie voor Wetenschappelijk Onderzoek 016.136.125Netherlands Ministry of Social Affairs and Employment KV 110016Rembrandt Institute of Cardiovascular ScienceRijksinstituut voor Volksgezondheid en Milieu S/133800/01
6 · The paper itself

Abstract

Disruption of circadian rhythm by means of shift work has been associated with cardiovascular disease in humans. However, causality and underlying mechanisms have not yet been established. In this study, we exposed hyperlipidemic APOE*3-Leiden.CETP mice to either regular light-dark cycles, weekly 6 hours phase advances or delays, or weekly alternating light-dark cycles (12 hours shifts), as a well-established model for shift work. We found that mice exposed to 15 weeks of alternating light-dark cycles displayed a striking increase in atherosclerosis, with an approximately twofold increase in lesion size and severity, while mice exposed to phase advances and delays showed a milder circadian disruption and no significant effect on atherosclerosis development. We observed a higher lesion macrophage content in mice exposed to alternating light-dark cycles without obvious changes in plasma lipids, suggesting involvement of the immune system. Moreover, while no changes in the number or activation status of circulating monocytes and other immune cells were observed, we identified increased markers for inflammation, oxidative stress, and chemoattraction in the vessel wall. Altogether, this is the first study to show that circadian disruption by shifting light-dark cycles directly aggravates atherosclerosis development.

Indexed as

AtherosclerosisPhotoperiodAnimalsAortaApolipoprotein E3Cholesterol Ester Transfer ProteinsCircadian RhythmCytokinesDiet, WesternFemaleInflammationMacrophagesMiceMice, TransgenicApolipoprotein E3apolipoprotein E3 (Leidein)CETP protein, humanCholesterol Ester Transfer ProteinsCytokinesatherosclerosischemokinescircadian rhythminflammationmonocytes

Identifiers

PMID31599473
PMCPMC6916424
OpenAlexW2979752345

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.