Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Understanding of the mechanisms underlying atherosclerotic disorders has evolved beyond the view of a progressive collection of lipids and cellular debris in the vascular wall. Current evidence has implicated inflammatory pathways as an important pathogenic mechanism in atherogenesis and plaque destabilization. Although not necessarily the primary event, inflammation and cytokine activation during plaque formation and destabilization may represent a common final pathway to various stimuli. Thus, it seems that not only 'new' risk factors, such as infections with various microorganisms, but also classic risk factors for cardiovascular disease, such as hyperlipidemia, hypertension and diabetes, may promote their atherogenic effects through inflammatory responses. Indeed, recent reports have suggested that traditional cardiovascular medications may attenuate atherogenesis and enhance plaque stability, at least partly through anti-inflammatory mechanisms. However, uncovering the inflammatory pathways in atherosclerosis has raised the possibility that newer treatment modalities should be more directly targeted against inflammatory mediators. Recently, a series of experimental studies have reported reduction of atherosclerosis by immunomodulatory therapy, such as chemokine blockade, interleukin-10 and immunization/vaccination against oxidized low-density lipoprotein and heat-shock protein. It is conceivable that some of these approaches will be tested clinically and, if successful, they could provide novel treatment strategies in coronary artery disease in humans.
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PMID:Inflammation in coronary artery disease: potential role for immunomodulatory therapy. 1629 1

Ankylosing spondylitis (AS) is a chronic inflammatory disease mainly affecting the spine and sacroiliac joints. Mediators such as macrophage migration inhibitory factor (MIF) and interleukin-10 (IL-10) are thought to be involved in several inflammatory conditions, including AS. Proinflammatory cytokines regulate the production of oxidative stress markers, such as nitric oxide (NO) and malondialdehyde (MDA). Although oxidative stress and lipid peroxidation have been reported in AS, the association of AS with commonly known oxidative stress markers and cytokines remains uncertain. We have therefore studied whether serum MIF levels are elevated in patients with AS and whether the levels correlate with oxidative stress markers and disease activity parameters. Twenty-five AS patients and 18 healthy controls participated in this study; subjects with hypertension, diabetes, hyperlipidemia, and obesity were excluded. The levels of acute phase reactants, serum levels of glucose, lipids, MIF, IL-10, NO and MDA were studied. Spinal mobility was assessed by the Bath Ankylosing Spondylitis Metrology Index (BASMI). Patients were also assessed using with the Bath Ankylosing Spondylitis Functional Index and the Bath Ankylosing Spondylitis Disease Activity Index. Age and sex distribution were found to be comparable between AS patients and controls (p > 0.05). Acute phase reactants and MIF levels were significantly higher (p < 0.05) and IL-10 levels were significantly lower (<0.001) in the AS patients than in controls. There was a significant correlation between BASMI and MIF levels in AS patients (r = 0.714, p < 0.001). Based on these results, MIF may be involved in the pathogenesis of the chronic inflammation in AS and, consequently, targeting MIF may be beneficial in preventing complications or in initiating early treatment of the disease.
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PMID:Evaluation of inflammation and oxidative stress in ankylosing spondylitis: a role for macrophage migration inhibitory factor. 1978 18

Atherosclerosis initiated by hyperlipidemia is modulated by immune cells in its development, progression, and rupture that results in thrombotic arterial occlusion leading to strokes and myocardial infarction. B cells initially thought to be atheroprotective provide opposing roles by their different subsets. Unlike B2 cells that are atherogenic, serosal B1a cells are atheroprotective by producing natural IgM antibodies that clear modified low-density lipoprotein and apoptotic and necrotic debris. In addition to natural IgM antibodies, B1a cells may act as regulatory B cells by producing the anti-inflammatory cytokine interleukin-10, which inhibits proinflammatory cytokines secreted by activated macrophages and T cells in atherosclerotic lesions. These findings suggest in vivo expansion of atheroprotective B1a cells as a potential therapeutic strategy to augment the benefits of lipid-lowering statin therapy.
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PMID:Protective role of natural IgM-producing B1a cells in atherosclerosis. 2284 41