Evidence map›Paper›PMID 27818938›Full record

ArticleMolecular metabolism2016

Modulation of ambient temperature promotes inflammation and initiates atherosclerosis in wild type C57BL/6 mice.

Daniel A Giles, Bhama Ramkhelawon, Elizabeth M Donelan, Traci E Stankiewicz, Susan B Hutchison, Rajib Mukherjee, Monica Cappelletti, Rebekah Karns, Christopher L Karp, Kathryn J Moore and 1 more

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

53 citing papers in PubMed, 81 citations in OpenAlex.

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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

11 authors at 4 institutions in 1 country.

Daniel A GilesDivision of Immunobiology, Cincinnati Children's Hospital Research Foundation, University of Cincinnati College of Medicine, Cincinnati, OH 45229, USA; Immunology Graduate Program, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH 45220, USA.
Bhama RamkhelawonDepartment of Medicine, Marc and Ruti Bell Program for Vascular Biology and Disease, The Leon H. Charney Division of Cardiology, New York University School of Medicine, New York, NY 10016, USA; Department of Surgery, New York University School of Medicine, New York, NY 10016, USA.
Elizabeth M DonelanDivision of Immunobiology, Cincinnati Children's Hospital Research Foundation, University of Cincinnati College of Medicine, Cincinnati, OH 45229, USA.
Traci E StankiewiczDivision of Immunobiology, Cincinnati Children's Hospital Research Foundation, University of Cincinnati College of Medicine, Cincinnati, OH 45229, USA.
Susan B HutchisonDepartment of Medicine, Marc and Ruti Bell Program for Vascular Biology and Disease, The Leon H. Charney Division of Cardiology, New York University School of Medicine, New York, NY 10016, USA.
Rajib MukherjeeDivision of Immunobiology, Cincinnati Children's Hospital Research Foundation, University of Cincinnati College of Medicine, Cincinnati, OH 45229, USA.
Monica CappellettiDivision of Immunobiology, Cincinnati Children's Hospital Research Foundation, University of Cincinnati College of Medicine, Cincinnati, OH 45229, USA.
Rebekah KarnsDivision of Gastroenterology, Hepatology and Nutrition, Cincinnati Children's Hospital Research Foundation, University of Cincinnati College of Medicine, Cincinnati, OH 45229, USA.
Christopher L KarpDiscovery & Translational Sciences, The Bill & Melinda Gates Foundation, Seattle, WA 98109, USA.
Kathryn J MooreDepartment of Medicine, Marc and Ruti Bell Program for Vascular Biology and Disease, The Leon H. Charney Division of Cardiology, New York University School of Medicine, New York, NY 10016, USA.
Senad DivanovicDivision of Immunobiology, Cincinnati Children's Hospital Research Foundation, University of Cincinnati College of Medicine, Cincinnati, OH 45229, USA; Immunology Graduate Program, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH 45220, USA. Electronic address: senad.divanovic@cchmc.org.
University of Cincinnati Medical Center · USCincinnati Children's Hospital Medical Center · USNew York University · USBill & Melinda Gates Foundation · US

Funding

REPRODUCTIVE AND DEVELOPMENTAL TOXICOLOGY RESEARCHP30ES006096 · NIEHS · UNIVERSITY OF CINCINNATI · PI YADAV, JAGJIT S · 1992 to 2022
$35.4M
Stem Cell/Organoid and Genome Editing CoreP30DK078392 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI LEE ARMISTEAD DENSON · 2007 to 2026
$24.4M
Immunopathogenesis of Non-alcoholic Fatty Liver DiseaseR01DK099222 · NIDDK · CINCINNATI CHILDRENS HOSP MED CTR · PI Senad Divanovic · 2013 to 2026
$5.6M
Pathogenesis and therapeutic targeting of immune disordersT32AI118697 · NIAID · CINCINNATI CHILDRENS HOSP MED CTR · PI HILDEMAN, DAVID A · 2016 to 2020
$683k
Better mouse models of disease: Humanizing experimental atherosclerosisR21HL113907 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI DIVANOVIC, SENAD · 2012 to 2013
$421k
Dysregulation of Neuronal Guidance Cue Netrin-1 in Accelerated AAAK99HL125667 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI RAMKHELAWON, BHAMA · 2015 to 2016
$221k
NHLBI NIH HHS K99 HL125667NHLBI NIH HHS R21 HL113907NIAID NIH HHS T32 AI118697NIDDK NIH HHS P30 DK078392NIDDK NIH HHS R01 DK099222NIEHS NIH HHS P30 ES006096
6 · The paper itself

Abstract

objectivesObesity and obesity-associated inflammation is central to a variety of end-organ sequelae including atherosclerosis, a leading cause of death worldwide. Although mouse models have provided important insights into the immunopathogenesis of various diseases, modeling atherosclerosis in mice has proven difficult. Specifically, wild-type (WT) mice are resistant to developing atherosclerosis, while commonly used genetically modified mouse models of atherosclerosis are poor mimics of human disease. The lack of a physiologically relevant experimental model of atherosclerosis has hindered the understanding of mechanisms regulating disease development and progression as well as the development of translational therapies. Recent evidence suggests that housing mice within their thermoneutral zone profoundly alters murine physiology, including both metabolic and immune processes. We hypothesized that thermoneutral housing would allow for augmentation of atherosclerosis induction and progression in mice.

methodsApoE

resultsHousing mice at T

conclusionsIn sum, our novel data in WT C57Bl/6 mice suggest that modulation of a single environmental variable, temperature, dramatically alters mouse physiology, metabolism, and inflammation, allowing for an improved mouse model of atherosclerosis. Thus, thermoneutral housing of mice shows promise in yielding a better understanding of the cellular and molecular pathways underlying the pathogenesis of diverse diseases.

Indexed as

InflammationTemperatureAnimalsAtherosclerosisHumansMiceMice, Inbred C57BLMice, KnockoutAtherosclerosisInflammationThermoneutrality

Identifiers

PMID27818938
PMCPMC5081423
OpenAlexW2521110133

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.