Immunity, atherosclerosis and cardiovascular disease
By J. Frostegård. BMC Medicine, 2013
976 citations recorded by the source corpus.
Atherosclerosis, the major cause of cardiovascular disease (CVD), is a chronic inflammatory condition with immune competent cells in lesions producing mainly pro-inflammatory cytokines. Dead cells and oxidized forms of low density lipoproteins (oxLDL) are abundant. The major direct cause of CVD appears to be rupture of atherosclerotic plaques. oxLDL has proinflammatory and immune-stimulatory properties, causes cell death at higher concentrations and contains inflammatory phospholipids with phosphorylcholine (PC) as an interesting epitope. Antibodies against PC (anti-PC) may be atheroprotective, one mechanism being anti-inflammatory. Bacteria and virus have been discussed, but it has been difficult to find direct evidence, and antibiotic trials have not been successful. Heat shock proteins could be one major target for atherogenic immune reactions. More direct causes of plaque rupture include pro-inflammatory cytokines, chemokines, and lipid mediators. To prove that inflammation is a cause of atherosclerosis and CVD, clinical studies with anti-inflammatory and/or immune-modulatory treatment are needed. The potential causes of immune reactions and inflammation in atherosclerosis and how inflammation can be targeted therapeutically to provide novel treatments for CVD are reviewed.
Subfields: Immunology, Molecular Biology, Rheumatology
View Paper: https://www.semanticscholar.org/paper/4a67810821725998d063b638cc30e199430cae7a
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Citations in the corpus
- NLRP3 Inflammasome and the IL-1 Pathway in Atherosclerosis. (2018, background): “erogenesis in an indirect manner by promoting local vascular as well as systemic inflammation.(21) However, despite pro-”
- Understanding the Holobiont: How microbial metabolites affect human health and shape the immune system (2017, background): “This destabilizes the entire plaque, facilitating rupture and subsequent formation of an embolus that may result in myocardial infarction, stroke, or other forms of cardiovascular disease (Brophy et al., 2017; Frostegård, 2013; Moore et al., 2013).”
- National lipid association recommendations for patient-centered management of dyslipidemia: part 1--full report. (2015, background): “After entering the arterial wall, the particles bind to proretentive extracellular molecules, become trapped, and are modified through oxidation and other processes, which increase their inflammatory properties and their unregulated uptake by macrophages.(40,42) As the macrophages become engorged wi”