ArticleCurrent cardiology reviews2017
Endotoxin, Toll-like Receptor-4, and Atherosclerotic Heart Disease.
Article in Current cardiology reviews, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 67 citations in OpenAlex.
- Article
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- Circulating Mycobiota Signatures and Cardiovascular Mortality among Patients Undergoing Hemodialysis.Journal of the American Society of Nephrology : JASN · 2026Article
- Xenobiotic Toxicants and Particulate Matter: Effects, Mechanisms, Impacts on Human Health, and Mitigation Strategies.Journal of xenobiotics · 2025Review
- Gut Microbiota, Microbial Metabolites, and Inflammation in Cardiac Surgery: Implications for Clinical Outcomes-A Narrative Review.Microorganisms · 2025Review
- Gut Microbiota in Heart Failure-The Role of Inflammation.Biomedicines · 2025Review
- Saturated fat in an evolutionary context.Lipids in health and disease · 2025Review
- Interactions between the gut microbiome, associated metabolites and the manifestation and progression of heart failure with preserved ejection fraction in ZSF1 rats.Cardiovascular diabetology · 2024Article
- Addressing the Missing Links in Cardiovascular Aging.Clinical interventions in aging · 2024Review
- Cardiometabolic Risk: Characteristics of the Intestinal Microbiome and the Role of Polyphenols.International journal of molecular sciences · 2023Review
- Association between lipid-A-producing oral bacteria of different potency and fractional exhaled nitric oxide in a Norwegian population-based adult cohort.Journal of translational medicine · 2023Article
- Gut Microbiota-Targeted Interventions in the Management of Chronic Kidney Disease.Seminars in nephrology · 2023Review
- Inhibition of TLR4 Alleviates Heat Stroke-Induced Cardiomyocyte Injury by Down-Regulating Inflammation and Ferroptosis.Molecules (Basel, Switzerland) · 2023Article
- Article
- Oxidized Low-density Lipoproteins and Lipopolysaccharides Augment Carotid Artery Plaque Vulnerability in Hypercholesterolemic Microswine.Cardiology and cardiovascular medicine · 2023Article
- Affinity and Inactivation of Bacterial Endotoxins for Medical Device Materials.Biomedical instrumentation & technology · 2023Article
- Lipopolysaccharides and Cellular Senescence: Involvement in Atherosclerosis.International journal of molecular sciences · 2022Review
- LPS and oxLDL-induced S100A12 and RAGE expression in carotid arteries of atherosclerotic Yucatan microswine.Molecular biology reports · 2022Article
- Quercetin Mitigates Endothelial Activation in a Novel Intestinal-Endothelial-Monocyte/Macrophage Coculture Setup.Inflammation · 2022Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEndotoxin is a lipopolysaccharide (LPS) constituent of the outer membrane of most gram negative bacteria. Ubiquitous in the environment, it has been implicated as a cause or contributing factor in several disparate disorders from sepsis to heatstroke and Type II diabetes mellitus. Starting at birth, the innate immune system develops cellular defense mechanisms against environmental microbes that are in part modulated through a series of receptors known as toll-like receptors. Endotoxin, often referred to as LPS, binds to toll-like receptor 4 (TLR4)/ myeloid differentiation protein 2 (MD2) complexes on various tissues including cells of the innate immune system, smooth muscle and endothelial cells of blood vessels including coronary arteries, and adipose tissue. Entry of LPS into the systemic circulation ultimately leads to intracellular transcription of several inflammatory mediators. The subsequent inflammation has been implicated in the development and progression atherosclerosis and subsequent coronary artery disease and heart failure.
objectiveThe potential roles of endotoxin and TLR4 are reviewed regarding their role in the pathogenesis of atherosclerotic heart disease.
conclusionAtherosclerosis is initiated by inflammation in arterial endothelial and subendothelial cells, and inflammatory processes are implicated in its progression to clinical heart disease. Endotoxin and TLR4 play a central role in the inflammatory process, and represent potential targets for therapeutic intervention. Therapy with HMG-CoA inhibitors may reduce the expression of TLR4 on monocytes. Other therapeutic interventions targeting TLR4 expression or function may prove beneficial in atherosclerotic disease prevention and treatment.
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