The L-type Ca2+ Channel as a Potential Mediator of Pathology During Alterations in Cellular Redox State

Heart Lung and Circulation

Volumn 18, Issue 1, 2009, Pages 3-10

  Hool, Livia C ^a  

^a UNIVERSITY OF WESTERN AUSTRALIA   (Australia)

Author keywords

Arrhythmia; Calcium; Hypertrophy; Hypoxia; L type calcium channel; Reactive oxygen species

Indexed keywords

CALCIUM CHANNEL L TYPE; HYDROGEN PEROXIDE; REACTIVE OXYGEN METABOLITE; SUPEROXIDE; CALCIUM; THIOL DERIVATIVE;

ARTICLE; CALCIUM CELL LEVEL; CALCIUM CHANNELOPATHY; CALCIUM CURRENT; CALCIUM HOMEOSTASIS; CELL HYPOXIA; CYTOPATHOLOGY; EVIDENCE BASED MEDICINE; HEART ARRHYTHMIA; HEART DEPOLARIZATION; HEART FUNCTION; HEART MUSCLE CELL; HEART MUSCLE FIBER MEMBRANE POTENTIAL; HEART VENTRICLE HYPERTROPHY; HUMAN; MYOCARDIUM PATHOLOGICAL REMODELLING; NONHUMAN; OXIDATION REDUCTION STATE; OXIDATIVE STRESS; PATHOPHYSIOLOGY; PRIORITY JOURNAL; SIGNAL TRANSDUCTION; ANIMAL; HEART VENTRICLE REMODELING; METABOLISM; OXIDATION REDUCTION REACTION; PATHOLOGY; REVIEW;

ANIMALS; ARRHYTHMIAS, CARDIAC; CALCIUM; CALCIUM CHANNELS, L-TYPE; HUMANS; HYDROGEN PEROXIDE; MYOCYTES, CARDIAC; OXIDATION-REDUCTION; SULFHYDRYL COMPOUNDS; SUPEROXIDES; VENTRICULAR REMODELING;

EID: 58949104727     PISSN: 14439506     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.hlc.2008.11.004     Document Type: Article

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