Vsevolod Polotsky

School of Medicine

Johns Hopkins University

Vsevolod Y. Polotsky

Dr. Vsevolod (Seva) Polotsky is an internationally recognized expert on the pathogenesis of obstructive sleep apnea and its metabolic complications. Dr. Polotsky received training in molecular biology and biochemistry at the NIH and Yale University. He has also been trained in pulmonary and sleep medicine at Johns Hopkins. During his pulmonary fellowship at the Johns Hopkins University he extensively studied ventilatory control and sleep in mice. His laboratory developed a mouse model of intermittent hypoxia (IH) mimicking the oxyhemoglobin profile in human OSA. Dr. Polotsky pioneered studies of glucose and lipid metabolism in IH. Dr. Polotsky has a track record of studying metabolic pathways in vivo and in vitro, breeding transgenic mice and using pharmacological inhibitors. He had continuous NIH funding since his graduation from pulmonary fellowship in 2002. He had published numerous papers in the field. Thus, Dr. Polotsky is a renowned expert in control of ventilation and the pathogenesis of sleep disordered breathing and its complications.

Dr. Polotsky’s research has been focused on several major areas. First, he studied the role of adipose tissue produced hormone leptin and its role in control of breathing and upper airway function. Second, he pioneered the chemogenetic approach to the pathogenesis of OSA demonstrating in the mouse model that pharyngeal patency can be manipulated remotely with designer receptors exclusively activated by designer drugs. Third, he has developed a mouse model of intermittent hypoxia (IH), which mimics the oxygen desaturation profile in human obstructive sleep apnea and provided the first evidence in the literature that IH causes insulin resistance. His later studies showed that IH increases hepatic glucose output acting via the carotid body-mediated activation of the sympathetic nervous system. Fourth, Dr. Polotsky provided the first evidence in the literature that IH induces dyslipidemia and atherosclerosis in mice. In follow up papers, Dr. Polotsky’s group identified mechanisms of dyslipidemia in IH, i.e. up-regulation of hepatic lipid biosynthesis and inhibition of lipoprotein clearance linked to inactivation of adipose lipoprotein lipase via hypoxia inducible factor 1 mediated up-regulation of angiopoietin-like 4. Fifth another Dr. Polotsky’s seminal finding that IH plays a role in the pathogenesis of liver injury and non-alcoholic fatty liver disease. Dr. Polotsky’s h-index in Google Scholar is 49.