Evidence map›Paper›PMID 21969583›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

Tissue-intrinsic dysfunction of circadian clock confers transplant arteriosclerosis.

Bo Cheng, Ciprian B Anea, Lin Yao, Feng Chen, Vijay Patel, Ana Merloiu, Paramita Pati, R William Caldwell, David J Fulton, R Daniel Rudic

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.2field-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

47 citing papers in PubMed, 76 citations in OpenAlex.

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  13. A wrinkle in time: circadian biology in pulmonary vascular health and disease.American journal of physiology. Lung cellular and molecular physiology · 2022
    Article
  14. Nuclear Receptors and Clock Components in Cardiovascular Diseases.International journal of molecular sciences · 2021
    Review
  15. Review: Circadian clocks and rhythms in the vascular tree.Current opinion in pharmacology · 2021
    Review
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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

10 authors at 3 institutions in 2 countries.

Bo ChengDepartment of Pharmacology and Toxicology, Vascular Biology Center, and Cardiothoracic and Vascular Surgery, Georgia Health Sciences University, Augusta, GA 30912, USA.
Ciprian B Anea
Lin Yao
Feng Chen
Vijay Patel
Ana Merloiu
Paramita Pati
R William Caldwell
David J Fulton
R Daniel Rudic
Augusta University Health · USCenter for Vascular Biology Research · USWuhan Union Hospital · CN

Funding

Therapeutic Mechanisms of RhoA Inhibition In Acute Lung InjuryP01HL101902 · NHLBI · AUGUSTA UNIVERSITY · PI VERIN, ALEXANDER D · 2011 to 2016
$11.2M
The biological clock, the endothelium, and vascular remodelingR01HL089576 · NHLBI · AUGUSTA UNIVERSITY · PI RUDIC, RADU DANIEL · 2008 to 2012
$2.1M
NHLBI NIH HHS HL089576NHLBI NIH HHS HL089576-01A1S1NHLBI NIH HHS P01 HL101902NHLBI NIH HHS R01 HL089576
6 · The paper itself

Abstract

The suprachiasmatic nucleus of the brain is the circadian center, relaying rhythmic environmental and behavioral information to peripheral tissues to control circadian physiology. As such, central clock dysfunction can alter systemic homeostasis to consequently impair peripheral physiology in a manner that is secondary to circadian malfunction. To determine the impact of circadian clock function in organ transplantation and dissect the influence of intrinsic tissue clocks versus extrinsic clocks, we implemented a blood vessel grafting approach to surgically assemble a chimeric mouse that was part wild-type (WT) and part circadian clock mutant. Arterial isografts from donor WT mice that had been anastamosed to common carotid arteries of recipient WT mice (WT:WT) exhibited no pathology in this syngeneic transplant strategy. Similarly, when WT grafts were anastamosed to mice with disrupted circadian clocks, the structural features of the WT grafts immersed in the milieu of circadian malfunction were normal and absent of lesions, comparable to WT:WT grafts. In contrast, aortic grafts from Bmal1 knockout (KO) or Period-2,3 double-KO mice transplanted into littermate control WT mice developed robust arteriosclerotic disease. These lesions observed in donor grafts of Bmal1-KO were associated with up-regulation in T-cell receptors, macrophages, and infiltrating cells in the vascular grafts, but were independent of hemodynamics and B and T cell-mediated immunity. These data demonstrate the significance of intrinsic tissue clocks as an autonomous influence in experimental models of arteriosclerotic disease, which may have implications with regard to the influence of circadian clock function in organ transplantation.

Indexed as

AnimalsAortaARNTL Transcription FactorsArteriosclerosisCarotid Artery, CommonCircadian ClocksMacrophagesMaleMiceMice, CongenicMice, Inbred C57BLMice, KnockoutMutationOrgan SpecificityPeriod Circadian ProteinsReceptors, Antigen, T-CellARNTL Transcription FactorsBmal1 protein, mousePer2 protein, mousePer3 protein, mousePeriod Circadian ProteinsReceptors, Antigen, T-Cell

Identifiers

PMID21969583
PMCPMC3193243
OpenAlexW1963590036

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.