L-type calcium channel: Clarifying the "oxygen sensing hypothesis".
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.
School of Anatomy, Physiology and Human Biology, University of Western Australia, Crawley, WA, Australia.
Henrietta
H
Cserne Szappanos
School of Anatomy, Physiology and Human Biology, University of Western Australia, Crawley, WA, Australia.
Helena
H
Viola
School of Anatomy, Physiology and Human Biology, University of Western Australia, Crawley, WA, Australia; Victor Chang Cardiac Research Institute, Sydney, NSW, Australia. Electronic address: livia.hool@uwa.edu.au.
Livia C
LC
Hool
D000818:Animals; D020746:Calcium Channels, L-Type / Q000737:chemistry / Q000235:genetics / Q000378:metabolism*; D005786:Gene Expression Regulation; D006801:Humans; D010100:Oxygen / Q000378:metabolism*
D020746:Calcium Channels, L-Type; D010100:Oxygen
Glutathionylation; Hypoxia; L-type calcium channel; Oxidative stress; Redox modification