“…17,18 Current evidence suggests that EMAP-II and its precursor (pro-EMAP-II/p43) stimulate the gene expression of proinflammatory cytokines, such as a TNF, IL-8, and IL-1, and increases circulating levels of TNF, IL-1, and IL-6, 19,20 which have been implicated in the progression of heat-related injuries. 12 Additionally, serum concentrations of EMAP-II have been shown to be elevated in individuals with micro-vascular complications, 21,22 potentially playing a role in endothelial dysfunction 23 and consequently affecting the body's ability to thermoregulate in individuals with T2D or HTN by attenuating cutaneous vasodilation or whole-body heat loss. 6,24 However, the relationships between EMAP-II, exercise (work), environmental heat, the presence of chronic disease, and the confounding effect of natural aging have yet to be explored in depth.…”