Calcium Release Channel of Sarcoplasmic Reticulum: An Important Target for Doxorubicin-Mediated Cardiotoxicity View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

1992

AUTHORS

Isaac N. Pessah

ABSTRACT

Sarcoplasmic reticulum (SR) of cardiac muscle makes essential contributions to excitation-contraction (E-C) coupling by regulating the free calcium (Ca2+) levels in the myoplasm. The ryanodine receptor constitutes the ligand-gated Ca2+ channel localized at junctional regions of SR through which Ca2+ is released in response to the action potential at the T tubule membrane. The ryanodine receptor complex appears to be co-associated with the voltage-dependent Ca2+ channels of the sarcolemma at the triad junction and the interaction of these proteins is critical to the process of E-C coupling. The role of triadic receptors in the etiology of drug-induced cardiomyopathy is explored. Doxorubicin and its anthraquinone (AQ) congeners are clinically valuable chemotherapeutic agents effective against a broad spectrum of human cancers. The repetitive doses of AQ required for control of malignancies coincides with induction of a progressive and irreversible cardiomyopathy which results in arrhythmias, tachycardia, declining ventricular output, and eventually congestive heart failure. Greater than 65% of patients receiving the maximal acceptable cumulative dosages of doxorubicin develop debilitating ventricular dysfunction. The etiology of AQ cardiomyopathy is unknown, but like genetic dilated cardiomyopathy, the drug-induced disease exhibits a similar progression of abnormal diastolic filling and impaired rates of ventricular relaxation. More... »

PAGES

409-410

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-1-4615-3362-7_58

DOI

http://dx.doi.org/10.1007/978-1-4615-3362-7_58

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1000978141

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/1326869


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