Journal
INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY
Volume 86, Issue -, Pages 32-36Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.biocel.2017.03.010
Keywords
L-type calcium channel; Redox modification; Hypoxia; Oxidative stress; Glutathionylation
Categories
Funding
- National Health and Medical Research Council of Australia [APP1010726, APP1041582, 634501]
- Australian Research Council [FT100100756]
- National Health and Medical Research Council [APP1002207, APP1117366]
- Australian Research Council [FT100100756] Funding Source: Australian Research Council
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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. (C) 2017 Elsevier Ltd. All rights reserved.
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