RT Generic
T1 Redox signaling in acute oxygen sensing.
A1 Gao, Lin
A1 Gonzalez-Rodriguez, Patricia
A1 Ortega-Saenz, Patricia
A1 Lopez-Barneo, Jose
K1 Acute oxygen sensing
K1 Adrenal medulla
K1 Carotid body
K1 Hypoxia
K1 Mitochondrial complex I
K1 Peripheral chemoreceptors
K1 Pyridine nucleotides
K1 Reactive oxygen species (ROS)
AB Acute oxygen (O2) sensing is essential for individuals to survive under hypoxic conditions. The carotid body (CB) is the main peripheral chemoreceptor, which contains excitable and O2-sensitive glomus cells with O2-regulated ion channels. Upon exposure to acute hypoxia, inhibition of K+ channels is the signal that triggers cell depolarization, transmitter release and activation of sensory fibers that stimulate the brainstem respiratory center to produce hyperventilation. The molecular mechanisms underlying O2 sensing by glomus cells have, however, remained elusive. Here we discuss recent data demonstrating that ablation of mitochondrial Ndufs2 gene selectively abolishes sensitivity of glomus cells to hypoxia, maintaining responsiveness to hypercapnia or hypoglycemia. These data suggest that reactive oxygen species and NADH generated in mitochondrial complex I during hypoxia are signaling molecules that modulate membrane K+ channels. We propose that the structural substrates for acute O2 sensing in CB glomus cells are "O2-sensing microdomains" formed by mitochondria and neighboring K+ channels in the plasma membrane.
PB Elsevier BV
YR 2017
FD 2017
LK http://hdl.handle.net/10668/11175
UL http://hdl.handle.net/10668/11175
LA en
NO Gao L, González-Rodríguez P, Ortega-Sáenz P, López-Barneo J. Redox signaling in acute oxygen sensing. Redox Biol. 2017 Aug;12:908-915.
DS RISalud
RD Jul 30, 2025