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Oxidative stress plays a critical role in the pathogenesis of various disorders including cardiovascular diseases, such as ischemia/reperfusion (I/R) injury, atherosclerosis, dyslipidemia, chronic kidney disease (CKD), arrhythmia, and diabetic cardiovascular complications. Although reactive oxygen species (ROS) have been proposed as the key mediator of oxidative stress-induced cell injury, antioxidant therapies have failed in clinical trials, raising the possibility that some unknown mechanism other than ROS may be involved. In 2015, we reported a novel apoptosis-inducing humoral factor in conditioned medium from cardiac myocytes subjected to hypoxia/ reoxygenation. This novel 69th tyrosine-sulfated eukaryotic translation initiation factor 5A (eIF5A) was rapidly secreted from cells in response to oxidative stress and then acted as an apoptosis-inducing ligand in an autocrine fashion. We termed the novel secreted form of eIF5A “Oxidative stress-Responsive Apoptosis-Inducing Protein” (ORAIP). Evidence has accumulated that ORAIP may be a common and dominant apoptosis-inducer among various cell types in response to different types of oxidative stress and is involved in a wide spectrum of acute and chronic disorders. Among them, here, I summarize knowledge regarding the possible roles of ORAIP in myocardial and cerebral I/R injury, dyslipidemia in terms of atherosclerosis, cardiovascular complications in diabetes mellitus,

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A novel and dominant factor that mediates oxidative stress-induced apoptotic signaling - autocrine/paracrine mechanism of the secreted form of eukaryotic translation initiation factor 5A