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European Heart Journal 1994 15(Supplement D):53-57; doi:10.1093/eurheartj/15.suppl_D.53
Copyright © 1994 by the European Society of Cardiology.
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© 1994 The European Society of Cardiology

Gap Junction Alterations in the Failing Heart

N. J. Severs

Department of Cardiac Medicine, National Heart and Lung Institute Dovehouse Street, London SW3 6LY, U.K.

Correspondence: Dr N. J. Severs, Department of Cardiac Medicine, National Heart and Lung Institute, Dovehouse Street, London SW3 6 LY, UK.

Electrical and mechanical integration between myocytes is mediated by three types of intercellular junction, the fascia adherens, desmosome and gap junction. Gap junctions are responsible for electrical coupling, and consist of clusters of plasma membrane channels that directly link the cytoplasmic compartments of neighbouring cells. Each channel consists of two hemichannels (connexons; one from each plasma membrane) aligned across the narrow extracellular gap, and each hemichannel is constructed from six connexin molecules. Using specific anticonnexin43 antibodies for immunofluorescence localization in combination with confocal laser scanning microscopy, alterations in the expression of connexin43 gap junctions have been investigated in chronic ischaemic heart disease and heart failure due to ischaemic cardiomyopathy. Two major alterations are apparent: (1) disturbance in the spatial distribution of gap junctions at the border zone of healed infarcts, and (2) reduction in the quantity of immunodetectable connexin43 in regions of normal gap junction distribution distant from infarct scars. These changes are likely to contribute to electromechanical dysfunction in ischaemic heart disease and heart failure, and appear to form part of a wider pattern of altered expression of different connexin types in the diseased heart.

Key Words: Heart failure • ischaemic heart disease • myocyte interaction • intercellular junctions • gap junction • intercalated disk • confocal microscopy • immunocytochemistry


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