Dataset related to the article: "BPIFB4 and its longevity-associated haplotype protect from cardiac ischemia in humans and mice"

Long-living individuals (LLIs) escape age-related cardiovascular complications until the very last stage of life. Previous studies haveshown that a Longevity-Associated Variant (LAV) of the BPI Fold Containing Family B Member 4 (BPIFB4) gene correlates with anextraordinarily prolonged life span. Moreover, delivery of the LAV-BPIFB4 gene exerted therapeutic action in murine models ofatherosclerosis, limb ischemia, diabetic cardiomyopathy, and aging. We hypothesize that downregulation of BPIFB4 expressionmarks the severity of coronary artery disease (CAD) in human subjects, and supplementation of the LAV-BPIFB4 protects the heartfrom ischemia. In an elderly cohort with acute myocardial infarction (MI), patients with three-vessel CAD were characterized bylower levels of the natural logarithm (Ln) of peripheral blood BPIFB4 (p = 0.0077). The inverse association between Ln BPIFB4 andthree-vessel CAD was confirmed by logistic regression adjusting for confounders (Odds Ratio = 0.81, p = 0.0054). Moreover, ininfarcted mice, a single administration of LAV-BPIFB4 rescued cardiac function and vascularization. In vitro studies showed that LAVBPIFB4protein supplementation exerted chronotropic and inotropic actions on induced pluripotent stem cell (iPSC)-derivedcardiomyocytes. In addition, LAV-BPIFB4 inhibited the pro-fibrotic phenotype in human cardiac fibroblasts. These findings provide astrong rationale and proof of concept evidence for treating CAD with the longevity BPIFB4 gene/protein.