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Pharmacological modulation of connexin-formed channels in cardiac pathophysiology

Elke De Vuyst (UGent) , Kerstin Boengler, Gudruun Antoons, Karin Sipido, Rainer Schulz and Luc Leybaert (UGent)
(2011) BRITISH JOURNAL OF PHARMACOLOGY. 163(3). p.469-483
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Abstract
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(+) , Ca(2+) 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.
Keywords
ANALOG ROTIGAPTIDE ZP123, SPONTANEOUS VENTRICULAR-ARRHYTHMIAS, GAP-JUNCTION, INTERCELLULAR COMMUNICATION, arrhythmia, cardiac ischaemia, connexins, gap junctions, hemichannels, peptides, MYOCARDIAL ISCHEMIA/REPERFUSION INJURY, REDUCES INFARCT SIZE, PROTEIN-KINASE-C, JUNCTION UNCOUPLER HEPTANOL, OPEN-CHEST DOGS, ANTIARRHYTHMIC PEPTIDE AAP10

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Citation

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MLA
De Vuyst, Elke, et al. “Pharmacological Modulation of Connexin-Formed Channels in Cardiac Pathophysiology.” BRITISH JOURNAL OF PHARMACOLOGY, vol. 163, no. 3, 2011, pp. 469–83.
APA
De Vuyst, E., Boengler, K., Antoons, G., Sipido, K., Schulz, R., & Leybaert, L. (2011). Pharmacological modulation of connexin-formed channels in cardiac pathophysiology. BRITISH JOURNAL OF PHARMACOLOGY, 163(3), 469–483.
Chicago author-date
De Vuyst, Elke, Kerstin Boengler, Gudruun Antoons, Karin Sipido, Rainer Schulz, and Luc Leybaert. 2011. “Pharmacological Modulation of Connexin-Formed Channels in Cardiac Pathophysiology.” BRITISH JOURNAL OF PHARMACOLOGY 163 (3): 469–83.
Chicago author-date (all authors)
De Vuyst, Elke, Kerstin Boengler, Gudruun Antoons, Karin Sipido, Rainer Schulz, and Luc Leybaert. 2011. “Pharmacological Modulation of Connexin-Formed Channels in Cardiac Pathophysiology.” BRITISH JOURNAL OF PHARMACOLOGY 163 (3): 469–483.
Vancouver
1.
De Vuyst E, Boengler K, Antoons G, Sipido K, Schulz R, Leybaert L. Pharmacological modulation of connexin-formed channels in cardiac pathophysiology. BRITISH JOURNAL OF PHARMACOLOGY. 2011;163(3):469–83.
IEEE
[1]
E. De Vuyst, K. Boengler, G. Antoons, K. Sipido, R. Schulz, and L. Leybaert, “Pharmacological modulation of connexin-formed channels in cardiac pathophysiology,” BRITISH JOURNAL OF PHARMACOLOGY, vol. 163, no. 3, pp. 469–483, 2011.
@article{1253117,
  abstract     = {{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(+) , Ca(2+) 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.}},
  author       = {{De Vuyst, Elke and Boengler, Kerstin and Antoons, Gudruun and Sipido, Karin and Schulz, Rainer and Leybaert, Luc}},
  issn         = {{0007-1188}},
  journal      = {{BRITISH JOURNAL OF PHARMACOLOGY}},
  keywords     = {{ANALOG ROTIGAPTIDE ZP123,SPONTANEOUS VENTRICULAR-ARRHYTHMIAS,GAP-JUNCTION,INTERCELLULAR COMMUNICATION,arrhythmia,cardiac ischaemia,connexins,gap junctions,hemichannels,peptides,MYOCARDIAL ISCHEMIA/REPERFUSION INJURY,REDUCES INFARCT SIZE,PROTEIN-KINASE-C,JUNCTION UNCOUPLER HEPTANOL,OPEN-CHEST DOGS,ANTIARRHYTHMIC PEPTIDE AAP10}},
  language     = {{eng}},
  number       = {{3}},
  pages        = {{469--483}},
  title        = {{Pharmacological modulation of connexin-formed channels in cardiac pathophysiology}},
  volume       = {{163}},
  year         = {{2011}},
}
Web of Science
Times cited: