TY - JOUR
T1 - L-type calcium channel
T2 - Clarifying the “oxygen sensing hypothesis”
AU - Cserne Szappanos, Henrietta
AU - Viola, Helena
AU - Hool, Livia C.
PY - 2017/5/1
Y1 - 2017/5/1
N2 - The heart is able to respond acutely to changes in oxygen tension. Since ion channels can respond rapidly to stimuli, the “ion channel oxygen sensing hypothesis” has been proposed to explain acute adaptation of cells to changes in oxygen demand. However the exact mechanism for oxygen sensing continues to be debated. Mitochondria consume the lion's share of oxygen in the heart, fuelling the production of ATP that drives excitation and contraction. Mitochondria also produce reactive oxygen species that are capable of altering the redox state of proteins. The cardiac L-type calcium channel is responsible for maintaining excitation and contraction. Recently, the reactive cysteine on the cardiac L-type calcium channel was identified. These data clarified that the channel does not respond directly to changes in oxygen tension, but rather responds to cellular redox state. This leads to acute alterations in cell signalling responsible for the development of arrhythmias and pathology.
AB - The heart is able to respond acutely to changes in oxygen tension. Since ion channels can respond rapidly to stimuli, the “ion channel oxygen sensing hypothesis” has been proposed to explain acute adaptation of cells to changes in oxygen demand. However the exact mechanism for oxygen sensing continues to be debated. Mitochondria consume the lion's share of oxygen in the heart, fuelling the production of ATP that drives excitation and contraction. Mitochondria also produce reactive oxygen species that are capable of altering the redox state of proteins. The cardiac L-type calcium channel is responsible for maintaining excitation and contraction. Recently, the reactive cysteine on the cardiac L-type calcium channel was identified. These data clarified that the channel does not respond directly to changes in oxygen tension, but rather responds to cellular redox state. This leads to acute alterations in cell signalling responsible for the development of arrhythmias and pathology.
KW - Glutathionylation
KW - Hypoxia
KW - L-type calcium channel
KW - Oxidative stress
KW - Redox modification
UR - http://www.scopus.com/inward/record.url?scp=85015891941&partnerID=8YFLogxK
U2 - 10.1016/j.biocel.2017.03.010
DO - 10.1016/j.biocel.2017.03.010
M3 - Short survey
C2 - 28323207
AN - SCOPUS:85015891941
SN - 1357-2725
VL - 86
SP - 32
EP - 36
JO - International Journal of Biochemistry and Cell Biology
JF - International Journal of Biochemistry and Cell Biology
ER -