Therefore, while our data provide robust proof-of-concept that SSAO inhibition is a novel and potent strategy against LPS-induced cardiac injury, the therapeutic efficacy of hydralazine must be validated in more clinically relevant models, such as polymicrobial sepsis (e.g., cecal ligation and puncture), and with clinically congruent treatment timelines, before any firm conclusions about its clinical utility can be drawn. This evidence concerns the gene AOC3 and Sepsis.