Downregulation of Immunodetectable Connexin43 and Decreased Gap Junction Size in the Pathogenesis of Chronic Hibernation in the Human Left Ventricle | Zendy

Raffi Kaprielian | Zendy; Mark Gunning | Zendy; E. Dupont | Zendy; Mary N. Sheppard | Zendy; Stephen Rothery | Zendy; Richard Underwood | Zendy; Dudley J. Pennell | Zendy; Keith A.A. Fox | Zendy; John Pepper | Zendy; Philip A. PooleWilson | Zendy; Nicholas J. Severs | Zendy

Open Access

Downregulation of Immunodetectable Connexin43 and Decreased Gap Junction Size in the Pathogenesis of Chronic Hibernation in the Human Left Ventricle

Author(s) -

Raffi Kaprielian,

Mark Gunning,

E. Dupont,

Mary N. Sheppard,

Stephen Rothery,

Richard Underwood,

Dudley J. Pennell,

Keith A.A. Fox,

John Pepper,

Philip A. PooleWilson,

Nicholas J. Severs

Publication year - 1998

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/01.cir.97.7.651

Subject(s) - ventricle , medicine , pathogenesis , ischemia , gap junction , cardiology , hibernation (computing) , hibernating myocardium , coronary artery disease , intracellular , myocardial infarction , biology , state (computer science) , revascularization , algorithm , computer science , microbiology and biotechnology

The regional wall motion impairment and predisposition to arrhythmias in human ventricular hibernation may plausibly result from abnormal intercellular propagation of the depolarizing wave front. This study investigated the hypothesis that altered patterns of expression of connexin43, the principal gap junctional protein responsible for passive conduction of the cardiac action potential, contribute to the pathogenesis of hibernation.

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