Studies on Hypoxic Pulmonary Vasoconstriction Detect a Novel Role for the Mitochondrial Complex i Subunit Ndufs2 in Controlling Peroxide Generation for Oxygen-Sensing

Abstract

The molecular mechanisms for the oxygen sensor that appears to be present in pulmonary arterial smooth muscle cells (PASMC) mediating hypoxic pulmonary vasoconstriction (HPV) have been the focus of extensive research and remain controversial.1,2 In this issue of Circulation Research, Dunham-Snary et al3 describe a novel involvement of the mitochondrial electron transport chain (ETC) rotenone binding site complex I subunit, Ndufs2 (NADH dehydrogenase [ubiquinone] iron-sulfur protein 2), in controlling an oxygendependent vasodilator source of peroxide generation that appears to contribute to acute HPV.