Review
The role of TNF-α in chronic inflammatory conditions, intermediary metabolism, and cardiovascular risk

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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-α (TNF-α) has been shown to play a key role in these processes and thus might be a potential therapeutic target. Increased concentrations of TNF-α 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-α 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-α blockade may improve insulin resistance and lipid profiles in patients with chronic inflammatory diseases.

tumor necrosis factor-α
lipids
anti-tumor necrosis factor
insulin resistance

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Published, JLR Papers in Press, January 2, 2007.

Abbreviations

    apoA-I

    apolipoprotein A-I

    ATGL

    adipocyte triglyceride lipase

    CETP

    cholesteryl ester transfer protein

    CYP7A1

    cholesterol-7α-hydroxylase

    DM

    diabetes mellitus

    HSL

    hormone-sensitive lipase

    IL-6

    interleukin-6

    IRS-1

    insulin receptor substrate-1

    JNK

    c-jun-NH2-terminal kinase

    LPS

    lipopolysaccharide

    RA

    rheumatoid arthritis

    RCT

    reverse cholesterol transport

    TG

    triglyceride

    TNF-α

    tumor necrosis factor-α

    TNF-RI

    tumor necrosis factor receptor type I