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Pharmacological modulation of connexin‐formed channels in cardiac pathophysiology

British journal of pharmacology, 2011-06, Vol.163 (3), p.469-483 [Peer Reviewed Journal]

2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society ;2015 INIST-CNRS ;2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society. ;British Journal of Pharmacology © 2011 The British Pharmacological Society 2011 ;ISSN: 0007-1188 ;EISSN: 1476-5381 ;DOI: 10.1111/j.1476-5381.2011.01244.x ;PMID: 21265827 ;CODEN: BJPCBM

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Title:
Pharmacological modulation of connexin‐formed channels in cardiac pathophysiology
Author: De Vuyst, Elke ; Boengler, Kerstin ; Antoons, Gudrun ; Sipido, Karin R. ; Schulz, Rainer ; Leybaert, Luc
Subjects: Animals ; Anti-Arrhythmia Agents - adverse effects ; Anti-Arrhythmia Agents - pharmacology ; Anti-Arrhythmia Agents - therapeutic use ; arrhythmia ; Arrhythmias, Cardiac - drug therapy ; Arrhythmias, Cardiac - metabolism ; Arrhythmias, Cardiac - pathology ; Biological and medical sciences ; Cardiac arrhythmia ; Cardiac dysrhythmias ; cardiac ischaemia ; Cardiology. Vascular system ; Cardiomyocytes ; Clinical Trials as Topic ; connexins ; Connexins - physiology ; Drug therapy ; gap junctions ; Gap Junctions - physiology ; Heart ; Heart Diseases - drug therapy ; Heart Diseases - metabolism ; Heart Diseases - pathology ; hemichannels ; Humans ; Medical sciences ; Molecular Targeted Therapy ; Myocardial Infarction - drug therapy ; Myocardial Infarction - metabolism ; Myocardial Infarction - pathology ; Myocardial Ischemia - drug therapy ; Myocardial Ischemia - metabolism ; Myocardial Ischemia - pathology ; Myocardium - metabolism ; Myocardium - pathology ; peptides ; Peptides - adverse effects ; Peptides - pharmacology ; Peptides - therapeutic use ; Pharmacology. Drug treatments ; Reviews
Is Part Of: British journal of pharmacology, 2011-06, Vol.163 (3), p.469-483
Description: Coordinated electrical activity in the heart is supported by gap junction channels located at the intercalated discs of cardiomyocytes. Impaired gap junctional communication between neighbouring cardiomyocytes contributes to the development of re‐entry arrhythmias after myocardial ischaemia. Current antiarrhythmic therapy is hampered by a lack of efficiency and side effects, creating the need for a new generation of drugs. In this review, we focus on compounds that increase gap junctional communication, thereby increasing the conduction velocity and decreasing the risk of arrhythmias. Some of these compounds also inhibit connexin 43 (Cx43) hemichannels, thereby limiting adenosine triphosphate loss and volume overload following ischaemia/reperfusion, thus potentially increasing the survival of cardiomyocytes. The compounds discussed in this review are: (i) antiarrythmic peptide (AAP), AAP10, ZP123; (ii) GAP‐134; (iii) RXP‐E; and (vi) the Cx mimetic peptides Gap 26 and Gap 27. None of these compounds have effects on Na+, Ca2+ and K+ channels, and therefore have no proarrhythmic activity associated with currently available antiarrhythmic drugs. GAP‐134, RXP‐E, Gap 26 and Gap 27 are pharmalogical agents with a favorable clinical safety profile, as already confirmed in phase I clinical trials for GAP‐134. These agents show an excellent promise for treatment of arrhythmias in patients with ischaemic cardiomyopathy.
Publisher: Oxford, UK: Blackwell Publishing Ltd
Language: English
Identifier: ISSN: 0007-1188
EISSN: 1476-5381
DOI: 10.1111/j.1476-5381.2011.01244.x
PMID: 21265827
CODEN: BJPCBM
Source: Geneva Foundation Free Medical Journals at publisher websites
MEDLINE
PubMed Central
Alma/SFX Local Collection

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Pharmacological modulation of connexin‐formed channels in cardiac pathophysiology

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