Evidence map›Paper›PMID 29622163›Full record

ArticleJournal of the American College of Cardiology2018

Chlamydia and Lipids Engage a Common Signaling Pathway That Promotes Atherogenesis.

Shuang Chen, Kenichi Shimada, Timothy R Crother, Ebru Erbay, Prediman K Shah, Moshe Arditi

Abstract read
In one paragraph

Article in Journal of the American College of Cardiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

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  16. Microorganisms · 2019
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Shuang ChenDepartment of Pediatrics, Division of Pediatric Infectious Diseases and Immunology, Cedars-Sinai Medical Center, Los Angeles, California; Department of Biomedical Sciences, Infectious and Immunologic Diseases Research Center, Cedars-Sinai Medical Center, Los Angeles, California.
Kenichi ShimadaDepartment of Pediatrics, Division of Pediatric Infectious Diseases and Immunology, Cedars-Sinai Medical Center, Los Angeles, California; Department of Biomedical Sciences, Infectious and Immunologic Diseases Research Center, Cedars-Sinai Medical Center, Los Angeles, California.
Timothy R CrotherDepartment of Pediatrics, Division of Pediatric Infectious Diseases and Immunology, Cedars-Sinai Medical Center, Los Angeles, California; Department of Biomedical Sciences, Infectious and Immunologic Diseases Research Center, Cedars-Sinai Medical Center, Los Angeles, California.
Ebru ErbayDepartment of Biomedical Sciences, Infectious and Immunologic Diseases Research Center, Cedars-Sinai Medical Center, Los Angeles, California; Department of Medicine, Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California.
Prediman K ShahDivision of Cardiology, Oppenheimer Atherosclerosis Research Center, Cedars-Sinai Medical Center, Los Angeles, California.
Moshe ArditiDepartment of Pediatrics, Division of Pediatric Infectious Diseases and Immunology, Cedars-Sinai Medical Center, Los Angeles, California; Department of Biomedical Sciences, Infectious and Immunologic Diseases Research Center, Cedars-Sinai Medical Center, Los Angeles, California. Electronic address: moshe.arditi@cshs.org.
Cedars-Sinai Medical Center · US

Funding

MOLECULAR PATHOGENESIS OF CHLAMYDIA-INDUCED ATHEROGENESIR01HL066436 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI ARDITI, MOSHE · 2001 to 2013
$3.6M
Interaction with Rip2 and Th17 in Chronic InflammationR01AI117968 · NIAID · CEDARS-SINAI MEDICAL CENTER · PI ARDITI, MOSHE · 2016 to 2020
$2.3M
Innate Immunity and Pathogen mediated Acceleration in Vascular InflammationR01HL111483 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI CHEN, SHUANG · 2012 to 2016
$2.0M
NHLBI NIH HHS R01 HL066436NHLBI NIH HHS R01 HL111483NIAID NIH HHS R01 AI117968
6 · The paper itself

Abstract

backgroundRecent studies indicate that Toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88) signaling promote the development of high fat diet-induced atherosclerosis in hypercholesterolemic mice.

objectivesThe authors investigated the role of TLR4/MyD88 signaling in hematopoietic and stromal cells in the development and infection-mediated acceleration of atherosclerosis.

methodsThe authors generated bone marrow chimeras between wild-type and Tlr4

resultsAortic sinus plaques and lipid content were significantly reduced in Apoe

conclusionsThe authors show that both CP infection and metabolic stress associated with dyslipidemia use the same innate immune response pathway, utilizing TLR4/MyD88 signaling, with similar relative contributions in bone marrow-derived hematopoietic cells and in stromal cells. Further studies are required to understand this intricate and complex cross talk among innate and adaptive immune systems in various conditions to more effectively design dendritic cell-mediated atheroprotective vaccines and other therapeutic strategies.

Indexed as

Immunity, InnateLipid MetabolismLipidsAnimalsAtherosclerosisChlamydophila InfectionsChlamydophila pneumoniaeDisease Models, AnimalFemaleImmunohistochemistryMaleMiceMice, Inbred C57BLMice, KnockoutSignal TransductionLipidsatherosclerosisChlamydia pneumoniaedendritic cellsmyeloid differentiation factor 88Toll-like receptor 4

Identifiers

PMID29622163
PMCPMC6042865
OpenAlexW2795605419

What OpenQuestion holds

Textmetadata
LicenceTDM
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.