For instance, Prkar2b is the HIF-1α target gene [64] that influences synaptic function in neurons [65]; Adra2a regulates neurotransmitter release from sympathetic nerves and its elimination results in worsened cardiac function [66]; Brinp1 and Brinp2 are expressed in sympathetic neurons [67], and Brinp2 levels are altered after myocardial infarction [68]; and a member of the ephrin receptors, Epha5, is important for axon guidance, survival and neurite outgrowth of sympathetic neurons [69] were among downregulated transcripts. This evidence concerns the gene HIF1A and myocardial infarction.