L-type calcium channel: Clarifying the “oxygen sensing hypothesis”

Research output: Contribution to journalShort surveypeer-review

10 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)32-36
Number of pages5
JournalInternational Journal of Biochemistry and Cell Biology
Publication statusPublished - 1 May 2017


Dive into the research topics of 'L-type calcium channel: Clarifying the “oxygen sensing hypothesis”'. Together they form a unique fingerprint.

Cite this