Putative druggable targets for selective enhancement of cardiac conduction.
Putative druggable targets to selectively enhance cardiac conduction can be considered from the level of the ion channels determining the initiation and duration of the cardiac action potential to the gap junction proteins responsible for optimal cellular electrical coupling. Nature has provided a number of inherited disorders of conduction, the pathophysiology of which offer novel insights into future therapeutic targets. This review will focus upon the potential cellular and molecular targets for drug development based upon our knowledge of their pathophysiological impact.
Gomes
John
J
The Heart Hospital, University College Hospital & Institute of Cardiovascular Sciences, UCL, 16-18 Westmoreland Street, London W1G 8PH, United Kingdom.
Lambiase
Pier D
PD
D000818:Animals; D017487:Ankyrins / Q000502:physiology; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology* / Q000627:therapeutic use*; D053840:Brugada Syndrome / Q000188:drug therapy / Q000503:physiopathology; D016503:Drug Delivery Systems; D019204:GTP-Binding Proteins / Q000502:physiology; D017629:Gap Junctions / Q000187:drug effects / Q000502:physiology; D006321:Heart / Q000502:physiology* / Q000503:physiopathology*; D006329:Heart Conduction System / Q000502:physiology; D006801:Humans; D007473:Ion Channels / Q000187:drug effects / Q000503:physiopathology; D008133:Long QT Syndrome / Q000188:drug therapy; D009206:Myocardium / Q000378:metabolism; D015221:Potassium Channels / Q000502:physiology
D017487:Ankyrins; D000889:Anti-Arrhythmia Agents; D007473:Ion Channels; D015221:Potassium Channels; D019204:GTP-Binding Proteins