The role of TNF-alpha in chronic inflammatory conditions, intermediary metabolism, and cardiovascular risk.
SourceJournal of Lipid Research, 48, 4, (2007), pp. 751-62
Article / Letter to editor
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Journal of Lipid Research
SubjectIGMD 5: Health aging / healthy living; N4i 1: Pathogenesis and modulation of inflammation; N4i 2: Invasive mycoses and compromised host; N4i 4: Auto-immunity, transplantation and immunotherapy; NCEBP 14: Cardiovascular diseases; NCEBP 2: Evaluation of complex medical interventions; NCMLS 1: Immunity, infection and tissue repair; NCMLS 1: Infection and autoimmunity; UMCN 2.2: Vascular medicine and diabetes; UMCN 4.1: Microbial pathogenesis and host defense; UMCN 4.2: Chronic inflammation and autoimmunity; NCMLS 1: Infection and autoimmunity
The recent insight that inflammation contributes to the development of atherosclerosis and type 2 diabetes mellitus constitutes a major breakthrough in understanding the mechanisms underlying these conditions. In addition, it opens the way for new therapeutic approaches that might eventually decrease the prevalence of these public health problems. Tumor necrosis factor-alpha (TNF-alpha) has been shown to play a key role in these processes and thus might be a potential therapeutic target. Increased concentrations of TNF-alpha are found in acute and chronic inflammatory conditions (e.g., trauma, sepsis, infection, rheumatoid arthritis), in which a shift toward a proatherogenic lipid profile and impaired glucose tolerance occurs. Although therapeutic blockade of TNF-alpha worsens the prognosis in patients with abscesses and granulomatous infections, this strategy is highly beneficial in the case of chronic inflammatory conditions, including rheumatoid arthritis. Current investigations assessing the impact of anti-TNF agents on intermediary metabolism suggest that TNF-alpha blockade may improve insulin resistance and lipid profiles in patients with chronic inflammatory diseases.
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