Catalog Home Page

The cardiac L-type calcium channel alpha subunit is a target for direct redox modification during oxidative stress-the role of cysteine residues in the alpha interacting domain

Muralidharan, P., Cserne Szappanos, H., Ingley, E. and Hool, L.C. (2017) The cardiac L-type calcium channel alpha subunit is a target for direct redox modification during oxidative stress-the role of cysteine residues in the alpha interacting domain. Clinical and Experimental Pharmacology and Physiology, 44 (S1). pp. 46-54.

Free to read: https://doi.org/10.1111/1440-1681.12750
*No subscription required

Abstract

Cardiovascular disease is the leading cause of death in the Western world. The incidence of cardiovascular disease is predicted to further rise with the increase in obesity and diabetes and with the aging population. Even though the survival rate from ischaemic heart disease has improved over the past 30 years, many patients progress to a chronic pathological condition, known as cardiac hypertrophy that is associated with an increase in morbidity and mortality. Reactive oxygen species (ROS) and calcium play an essential role in mediating cardiac hypertrophy. The L-type calcium channel is the main route for calcium influx into cardiac myocytes. There is now good evidence for a direct role for the L-type calcium channel in the development of cardiac hypertrophy. Cysteines on the channel are targets for redox modification and glutathionylation of the channel can modulate the function of the channel protein leading to the onset of pathology. The cysteine responsible for modification of L-type calcium channel function has now been identified. Detailed understanding of the role of cysteines as possible targets during oxidative stress may assist in designing therapy to prevent the development of hypertrophy and heart failure.

Publication Type: Journal Article
Murdoch Affiliation: School of Veterinary and Life Sciences
Publisher: Wiley
Copyright: © 2017 John Wiley & Sons Australia, Ltd
URI: http://researchrepository.murdoch.edu.au/id/eprint/38635
Item Control Page Item Control Page