ArticleCell metabolism2018
Chlamydia pneumoniae Hijacks a Host Autoregulatory IL-1β Loop to Drive Foam Cell Formation and Accelerate Atherosclerosis.
Registry-linked trialOpen access · bronzeAbstract read
In one paragraph
Article in Cell metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06935279 (Bacteria in Atherosclerotic Plaques and Adverse Events), which is not on this map. Cited by 42 papers.
0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.1field-weighted citation impact, top 7% of its field
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.
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.
Bacteria in Atherosclerotic Plaques and Adverse Events
Who cites it
42 citing papers in PubMed, 91 citations in OpenAlex.
- Identification of Chlamydia pneumoniae and NLRP3 inflammasome activation in Alzheimer's disease retina.Nature communications · 2026Article
- Review
- Induction of LY6E regulates interleukin-1β production, potentially contributing to the immunopathogenesis of systemic lupus erythematosus.Cell communication and signaling : CCS · 2025Article
- Research progress of stem cells in the treatment of atherosclerosis.Frontiers in cell and developmental biology · 2025Review
- Association between dietary B vitamins intake and age-specific blood pressure: A cross-sectional study in American adults.PloS one · 2025Article
- Insufficient CXCL13 secretion in leprosy foamy macrophages attenuates lymphocyte recruitment and antimicrobial protein production.Frontiers in immunology · 2025Article
- IFN-γ induced the formation of foamy macrophages via CD40 signal to controlFrontiers in immunology · 2025Article
- TUDCA alleviates atherosclerosis by inhibiting AIM2 inflammasome and enhancing cholesterol efflux capacity in macrophage.iScience · 2024Article
- Universal cell membrane camouflaged nano-prodrugs with right-side-out orientation adapting for positive pathological vascular remodeling in atherosclerosis.Chemical science · 2024Article
- Inflammatory corpuscle AIM2 facilitates macrophage foam cell formation by inhibiting cholesterol efflux protein ABCA1.Scientific reports · 2024Article
- Review
- Insights into innate immune cell evasion byFrontiers in immunology · 2024Review
- Oxidative stress biomarker triggered multiplexed tool for auxiliary diagnosis of atherosclerosis.Science advances · 2023Article
- Recent Advances in Anti-Atherosclerosis and Potential Therapeutic Targets for Nanomaterial-Derived Drug Formulations.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Review
- Biomimetic nanoparticles targeting atherosclerosis for diagnosis and therapy.Smart medicine · 2023Review
- Genetic dissection of the impact of lncRNA AI662270 during the development of atherosclerosis.Journal of translational medicine · 2023Article
- The cause-and-effect relationship between gut microbiota abundance and carcinoid syndrome: a bidirectional Mendelian randomization study.Frontiers in microbiology · 2023Article
- Crosstalk Between Cholesterol, ABC Transporters, and PIP2 in Inflammation and Atherosclerosis.Advances in experimental medicine and biology · 2023Article
- Short-chain fatty acids are potential goalkeepers of atherosclerosis.Frontiers in pharmacology · 2023Review
- STAT3 Inhibits Autocrine IFN Signaling in Type I Conventional Dendritic Cells.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Gantsetseg TumurkhuuDepartments of Pediatrics and Medicine, Division of Infectious Diseases and Immunology, and Infectious and Immunologic Diseases Research Center (IIDRC), Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Jargalsaikhan DagvadorjDepartments of Pediatrics and Medicine, Division of Infectious Diseases and Immunology, and Infectious and Immunologic Diseases Research Center (IIDRC), Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Rebecca A PorrittDepartments of Pediatrics and Medicine, Division of Infectious Diseases and Immunology, and Infectious and Immunologic Diseases Research Center (IIDRC), Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Timothy R CrotherDepartments of Pediatrics and Medicine, Division of Infectious Diseases and Immunology, and Infectious and Immunologic Diseases Research Center (IIDRC), Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Kenichi ShimadaDepartments of Pediatrics and Medicine, Division of Infectious Diseases and Immunology, and Infectious and Immunologic Diseases Research Center (IIDRC), Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Elizabeth J TarlingDepartment of Medicine, Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Ebru ErbayDepartment of Molecular Biology and Genetics and National Nanotechnology Center, Bilkent University, Ankara, Turkey.
Moshe ArditiDepartments of Pediatrics and Medicine, Division of Infectious Diseases and Immunology, and Infectious and Immunologic Diseases Research Center (IIDRC), Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA. Electronic address: moshe.arditi@cshs.org.
Shuang ChenDepartments of Pediatrics and Medicine, Division of Infectious Diseases and Immunology, and Infectious and Immunologic Diseases Research Center (IIDRC), Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Cedars-Sinai Medical Center · USBilkent University · TRUniversity of California, Los Angeles · US
Funding
MOLECULAR PATHOGENESIS OF CHLAMYDIA-INDUCED ATHEROGENESIR01HL066436 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI ARDITI, MOSHE · 2001 to 2013
$3.6MInteraction with Rip2 and Th17 in Chronic InflammationR01AI117968 · NIAID · CEDARS-SINAI MEDICAL CENTER · PI ARDITI, MOSHE · 2016 to 2020
$2.3MInnate Immunity and Pathogen mediated Acceleration in Vascular InflammationR01HL111483 · NHLBI · CEDARS-SINAI MEDICAL CENTER · PI CHEN, SHUANG · 2012 to 2016
$2.0MPost-Translational Regulation of Lipid MetabolismR01HL136543 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TARLING, ELIZABETH JOANNA · 2017 to 2021
$1.9MRole of ABCG1 in lipid homeostasis, inflammation and innate immunityR00HL118161 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TARLING, ELIZABETH JOANNA · 2015 to 2017
$740kMitochondrial DNA Damage and Inflammasome Activation in Vascular InflammationR21AI105845 · NIAID · CEDARS-SINAI MEDICAL CENTER · PI ARDITI, MOSHE · 2014 to 2015
$459kNHLBI NIH HHS R00 HL118161NHLBI NIH HHS R01 HL066436NHLBI NIH HHS R01 HL111483NHLBI NIH HHS R01 HL136543NIAID NIH HHS R01 AI117968NIAID NIH HHS R21 AI105845
Abstract
Pathogen burden accelerates atherosclerosis, but the mechanisms remain unresolved. Activation of the NLRP3 inflammasome is linked to atherogenesis. Here we investigated whether Chlamydia pneumoniae (C.pn) infection engages NLRP3 in promoting atherosclerosis. C.pn potentiated hyperlipidemia-induced inflammasome activity in cultured macrophages and in foam cells in atherosclerotic lesions of Ldlr
Indexed as
AnimalsAtherosclerosisATP Binding Cassette Transporter 1Biological TransportCaspase 1Chlamydophila pneumoniaeCholesterolFemaleFoam CellsHost Microbial InteractionsInflammasomesInterleukin-1betaMaleMiceMice, Inbred C57BLMice, KnockoutAbca1 protein, mouseATP Binding Cassette Transporter 1Casp1 protein, mouseCaspase 1CholesterolHcar2 protein, mouseIL1B protein, mouseInflammasomesInterleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseReceptors, G-Protein-CoupledABCA1aspartateatherosclerosischolesterol effluxC. pneumoniaefoam cellsGpr109ainterleukin-1 betaniacinNlrp3
Identifiers
What Socratic holds
Textmetadata
LicenceTDM
Read underepoch 390
Registered trials
NCT06935279ClinicalTrials.gov
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 Socratic graph.