Myocardial gap junctions: targets for novel approaches in the prevention of life-threatening cardiac arrhytmias

Title:

Myocardial gap junctions: targets for novel approaches in the prevention of life-threatening cardiac arrhytmias

Creator:

Narcisa Tribulová, Knezl, V., Ľudmila Okruhlicová, and Ján Slezák

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:97726471-7f78-4607-a6a8-7b55e707427e
uuid:97726471-7f78-4607-a6a8-7b55e707427e
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, kardiovaskulární fyziologie, fibrilace srdce, terapeutické aspekty, cardiovascular physiology, heart fibrillation, therapeutic aspects, atrial and ventricular fibrilation, gap junction, connexin channel, therapeutic targets, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

Direct cell-to-cell communication in the heart is maintained via gap junction channels composed of proteins termed connexins. Connexin channels ensure molecular and electrical signals propagation and hence are crucial in myocardial synchronization and heart function. Disease-induced gap junctions remodeling and/or an impairment or even block of intercellular communication due to acute pathological conditions results in derangements of myocardial conduction and synchronization. This is critical in the development of both ventricular fibrillation, which is a major cause of sudden cardiac death and persistent atrial fibrillation, most common arrhythmia in clinical practice often resulting in stroke. Many studies suggest that alterations in topology (remodeling), expression, phosphorylation and particularly function of connexin channels due to age or disease are implicated in the development of these life-threatening arrhythmias. It seems therefore challenging to examine whether compounds that could prevent or attenuate gap junctions remodeling and connex in channels dysfunction can protect the heart against arrhythmias that cause sudden death in humans. This assumption is supported by very recent findings showing that an increase of gap junctional conductance by specific peptides can prevents atrial conduction slowing or re-entrant ventricular tachycardia in ischemic heart. Suppression of ischemia-induced dephosphorylation of connexin seems to be one of the mechanisms involved. Another approach for identifying novel treatments is based on the hypothesis that even non-antiarrhythmic drugs with antiarrhythmic ability can modulate gap junctional communication and hence attenuate arrhythmogenic substrates., N. Tribulová, V. Knezl, Ľ. Okruhlicová, J. Slezák., and Obsahuje bibliografii a bibliografické odkazy

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2008 Volume:57 | Number:Suppl 2

Harvested from:

CDK

Metadata only:

false