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Burn wound progression is complex and caused by additive effects of inadequate tissue perfusion, free radical damage, and systemic alterations in the cytokine milieu of burn patients, leading to protein denaturation and necrosis. Even though insufficient evidence exists for causal inferences, infection, tissue desiccation, edema, circumferential eschar, impaired wound perfusion, metabolic derangements, advanced age, and poor general health play important roles. Although consensus-building research is ongoing, current mainstays of treatment include adequate fluid resuscitation, nutritional support, and local wound care, with an emphasis on topical antimicrobial agents and biosynthetic dressings. Identifying early indicators by elucidating possible interacting or synergistic mechanisms and by developing preventative strategies will enhance prevention and treatment.

Insulin and insulin-like growth factors (IGFs) maintain vital neuronal functions. Absolute or functional deficiencies of insulin or IGF-I may contribute to neuronal and vascular complications associated with diabetes. Vanilloid receptor 1 (also called TRPV1) is an ion channel that mediates inflammatory thermal nociception and is present on sensory neurons. Here we demonstrate that both insulin and IGF-I enhance TRPV1-mediated membrane currents in heterologous expression systems and cultured dorsal root ganglion neurons. Enhancement of membrane current results from both increased sensitivity of the receptor and translocation of TRPV1 from cytosol to plasma membrane. Receptor tyrosine kinases trigger a signaling cascade leading to activation of phosphatidylinositol 3-kinase (PI(3)K) and protein kinase C (PKC)-mediated phosphorylation of TRPV1, which is found to be essential for the potentiation. These findings establish a link between the insulin family of trophic factors and vanilloid receptors.

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