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

Research output: Contribution to journalShort survey

4 Citations (Scopus)

Abstract

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
Volume86
DOIs
Publication statusPublished - 1 May 2017

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L-Type Calcium Channels
Oxygen
Mitochondria
Ion Channels
Oxidation-Reduction
Cell signaling
Fueling
Pathology
Cysteine
Reactive Oxygen Species
Adenosine Triphosphate
Cardiac Arrhythmias
Proteins

Cite this

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title = "L-type calcium channel: Clarifying the “oxygen sensing hypothesis”",
abstract = "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.",
keywords = "Glutathionylation, Hypoxia, L-type calcium channel, Oxidative stress, Redox modification",
author = "{Cserne Szappanos}, Henrietta and Helena Viola and Hool, {Livia C.}",
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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

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