We are analyzing https://link.springer.com/article/10.1007/s00018-020-03453-7.

Title:
Infection and atherosclerosis: TLR-dependent pathways | Cellular and Molecular Life Sciences
Description:
Atherosclerotic vascular disease (ASVD) is a chronic process, with a progressive course over many years, but it can cause acute clinical events, including acute coronary syndromes (ACS), myocardial infarction (MI) and stroke. In addition to a series of typical risk factors for atherosclerosis, like hyperlipidemia, hypertension, smoking and obesity, emerging evidence suggests that atherosclerosis is a chronic inflammatory disease, suggesting that chronic infection plays an important role in the development of atherosclerosis. Toll-like receptors (TLRs) are the most characteristic members of pattern recognition receptors (PRRs), which play an important role in innate immune mechanism. TLRs play different roles in different stages of infection of atherosclerosis-related pathogens such as Chlamydia pneumoniae (C. pneumoniae), periodontal pathogens including Porphyromonas gingivalis (P. gingivalis), Helicobacter pylori (H. pylori) and human immunodeficiency virus (HIV). Overall, activation of TLR2 and 4 seems to have a profound impact on infection-related atherosclerosis. This article reviews the role of TLRs in the process of atherosclerosis after C. pneumoniae and other infections and the current status of treatment, with a view to providing a new direction and potential therapeutic targets for the study of ASVD.
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Keywords {🔍}

pubmed, atherosclerosis, tlr, google, scholar, cas, infection, mice, tlrs, cells, central, pylori, pneumoniae, tolllike, receptor, role, cell, signaling, atherosclerotic, hiv, activation, reported, gingivalis, disease, inflammatory, human, treatment, expression, pathway, studies, receptors, immune, formation, protein, chlamydia, pathogens, addition, vascular, development, progression, plaque, chronic, inflammation, gut, coronary, risk, helicobacter, lps, apoe, patients,

Topics {✒️}

c5ar-tlr2 cross-talk involving macrophage receptors sr-a1 hospital-based case–control study oxidized low-density lipoprotein nlrp3-il1β signaling pathway mitogen-activated protein kinase secrete interferon-alpha heat-shock protein groel platelet-derived growth factor upstream serine/threonine kinase tauro-beta-muricholic acid trif-related adaptor molecule gram-negative anaerobic bacterium erythromycin resistance-forming modification article download pdf acute-phase protein c3 trif-dependent pathway responsible resembling hiv-mediated pathology p38-map kinase signal egfr/tlr3-dependent manner siv-infected rhesus monkeys canonical tank-binding-kinase 1 apolipoprotein e-deficient mice gram-negative anaerobic organism gut microbiota profiles helicobacter pylori-induced gastritis tumor necrosis factor tlr2/4/myd88-dependent manner induce pre-inflammatory cytokines late trif-dependent pathways diet-induced hyperlipidemic mice tlr2-tlr6 heterodimer contributed yuanpeng xia central nervous system foam cell formation foam cells induced myd88-dependent tlr4 signaling alveolar bone resorption endothelium-dependent relaxation damage promoting foam formation receptor-mediated immune responses herpes simplex virus-1 herpes simplex virus-2 janeway ca jr inhibiting tlr-dependent signals c57bl/6j mice fed triggering nf-κb translocation simian immunodeficiency virus doxycycline affects diet outer sheath components

Questions {❓}

Amar S, Wu SC, Madan M (2009) Is Porphyromonas gingivalis cell invasion required for atherogenesis?
Is it the microbe itself or the myriad of signaling pathways, including TLRs that are activated in chronic infections, which ultimately lead to atherosclerosis?
Lockhart PB et al (2012) Periodontal disease and atherosclerotic vascular disease: does the evidence support an independent association?

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      headline:Infection and atherosclerosis: TLR-dependent pathways
      description:Atherosclerotic vascular disease (ASVD) is a chronic process, with a progressive course over many years, but it can cause acute clinical events, including acute coronary syndromes (ACS), myocardial infarction (MI) and stroke. In addition to a series of typical risk factors for atherosclerosis, like hyperlipidemia, hypertension, smoking and obesity, emerging evidence suggests that atherosclerosis is a chronic inflammatory disease, suggesting that chronic infection plays an important role in the development of atherosclerosis. Toll-like receptors (TLRs) are the most characteristic members of pattern recognition receptors (PRRs), which play an important role in innate immune mechanism. TLRs play different roles in different stages of infection of atherosclerosis-related pathogens such as Chlamydia pneumoniae (C. pneumoniae), periodontal pathogens including Porphyromonas gingivalis (P. gingivalis), Helicobacter pylori (H. pylori) and human immunodeficiency virus (HIV). Overall, activation of TLR2 and 4 seems to have a profound impact on infection-related atherosclerosis. This article reviews the role of TLRs in the process of atherosclerosis after C. pneumoniae and other infections and the current status of treatment, with a view to providing a new direction and potential therapeutic targets for the study of ASVD.
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