EA also increases brain-derived neurotrophic factor expression in heat stroke [28], modulates the NF-E2 related factor 2/antioxidant response element pathway to provide protection against endotoxic shock-induced acute lung injury [29], and inhibits the ERK1/2-Egr-1 signaling pathway, thereby protecting cardiomyocytes in a mouse model of myocardial ischemia − reperfusion [30]. Here, EGR1 is linked to acute lung injury.