Sanjiv Kaul

This paper develops a population PK/PD model to simulate the effects of VC108, a GPR39 inhibitor, on myocardial oxygen tension during acute myocardial infarction and reperfusion.

Single intravenous bolus of the GPR39 antagonist VC108 shrank infarct and no-reflow volumes in rat myocardial infarction when given before reperfusion, but not 30 min after reperfusion.

This paper identifies GPR39 and 15-HETE as key regulators of coronary autoregulation through in vivo experiments and metabolomic analysis in dogs.

This study shows that deleting GPR39 prevents pulmonary arterial hypertension by reducing hypoxia-induced signaling and vascular remodeling.

This study shows that gene conversion and NHEJ are major DNA repair mechanisms in human embryos, with gene conversion potentially useful for gene correction but also causing extensive loss of heterozygosity.

The paper identifies GPR39 as a microvascular smooth muscle cell receptor regulated by opposing eicosanoids, 15-HETE and 14,15-EET, which modulate coronary vascular resistance through distinct mechanisms.