Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28476010
.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Redox+Biol
2017 ; 12
(ä): 908-915
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Redox signaling in acute oxygen sensing
#MMPMID28476010
Gao L
; González-Rodríguez P
; Ortega-Sáenz P
; López-Barneo J
Redox Biol
2017[Aug]; 12
(ä): 908-915
PMID28476010
show ga
Acute oxygen (O(2)) sensing is essential for individuals to survive under hypoxic
conditions. The carotid body (CB) is the main peripheral chemoreceptor, which
contains excitable and O(2)-sensitive glomus cells with O(2)-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 O(2) 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 O(2)
sensing in CB glomus cells are "O(2)-sensing microdomains" formed by mitochondria
and neighboring K(+) channels in the plasma membrane.
free
free
free
