ArticlePathogens and disease2013
Chlamydia pneumoniae induces expression of pro-atherogenic factors through activation of the lectin-like oxidized LDL receptor-1.
Article in Pathogens and disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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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.
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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.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- Chlamydia pneumoniae-Mediated Inflammation in Atherosclerosis: A Meta-Analysis.Mediators of inflammation · 2015Pooled it
- Modulation of lectin-like oxidized low-density lipoprotein receptor-1 byJournal of dental sciences · 2025Article
- Elevated plasma soluble lectin-like oxidised low-density lipoprotein receptor 1 as an independent prognostic biomarker in sepsis.Lipids in health and disease · 2025Article
- Current Status of Primary, Secondary, and Tertiary Prevention of Coronary Artery Disease.The International journal of angiology : official publication of the International College of Angiology, Inc · 2021Review
- LOX-1 RegulatesFrontiers in cell and developmental biology · 2020Article
- Polyphenols fromMedChemComm · 2018Article
- Infectious Agents in Atherosclerotic Cardiovascular Diseases through Oxidative Stress.International journal of molecular sciences · 2017Review
- Manipulation of Host Cholesterol by Obligate Intracellular Bacteria.Frontiers in cellular and infection microbiology · 2017Review
- Biophysical regulation of Chlamydia pneumoniae-infected monocyte recruitment to atherosclerotic foci.Scientific reports · 2016Article
- Infection and Atherosclerosis Development.Archives of medical research · 2015Review
- Infection with Chlamydia pneumoniae as a cause of coronary heart disease: the hypothesis is still untested.Pathogens and disease · 2015Review
- Distinct gene signatures in aortic tissue from ApoE-/- mice exposed to pathogens or Western diet.BMC genomics · 2014Article
- Activated human mast cells induce LOX-1-specific scavenger receptor expression in human monocyte-derived macrophages.PloS one · 2014Article
- Early Trypanosoma cruzi infection reprograms human epithelial cells.BioMed research international · 2014Article
- GroEL1, a heat shock protein 60 of Chlamydia pneumoniae, impairs neovascularization by decreasing endothelial progenitor cell function.PloS one · 2013Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Several lines of evidence have associated Chlamydia pneumoniae with cardiovascular disease including acceleration of atherosclerotic lesion progression in hyperlipidemic animal models by infection. Many of the pro-atherogenic effects of oxidized low-density lipoprotein (ox-LDL) occur through the activation of the lectin-like ox-LDL receptor-1 (LOX-1). Chlamydia pneumoniae upregulates the expression of the LOX-1 mRNA, promotes the uptake of ox-LDL, and utilizes the LOX-1 receptor for infectivity. The overall goal of this study was to determine whether C. pneumoniae organisms upregulated LOX-1 protein expression in vascular cells and whether upregulation of pro-atherogenic factors by C. pneumoniae occurred through LOX-1. Chlamydia pneumoniae induced LOX-1 protein expression in both endothelial cells and RAW macrophages. Upregulation was prevented by preincubation of cells with LOX-1 antibody prior to infection. Similarly, C. pneumoniae upregulated protein expression of adhesion molecules, MMP-1, and MMP-3, which was mitigated by anti-LOX-1 antibody. Prior treatment of organisms with PNGase, which removes the chlamydial glycan that is N-linked to the major outer membrane, abolished C. pneumoniae upregulation of LOX-1. These studies suggest that activation of LOX-1 expression occurs through binding of the chlamydial glycan and provides one mechanism by which C. pneumoniae infection could play a role in the pathogenesis of atherosclerosis.
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Registered trials
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.