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Divergent Relationships Among Soluble Tumor Necrosis Factor-α Receptors 1 and 2, Insulin Resistance, and Endothelial Function

Inflammation has the capacity to impair flow-mediated vasodilatation, which is regarded as a causal factor in the development of atherosclerosis (1). Tumor necrosis factor-α (TNF-α) is a proinflammatory cytokine that is also implicated in the pathogenesis of insulin resistance and endothelium dysfunction linked to this event (2). Contradictory effects of TNF-α on endothelial function have been described in different studies (3). Acute intrabrachial TNF-α infusion impairs endothelium-dependent vasodilatation, but TNF-α also enhances protective mechanism (3).

After binding of TNF-α to TNF-α receptors (TNFR1 and TNFR2), a proteolytic cleavage of the extracellular parts of these receptor elicits the soluble forms, named sTNFR1 and sTNFR2 (4 …