Document Detail


Apoptosis in Anthracycline Cardiomyopathy.
MedLine Citation:
PMID:  22212952     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Apoptosis is a tightly regulated physiologic process of programmed cell death that occurs in both normal and pathologic tissues. Numerous in vitro or in vivo studies have indicated that cardiomyocyte death through apoptosis and necrosis is a primary contributor to the progression of anthracycline-induced cardiomyopathy. There are now several pieces of evidence to suggest that activation of intrinsic and extrinsic apoptotic pathways contribute to anthracycline-induced apoptosis in the heart. Novel strategies were developed to address a wide variety of cardiotoxic mechanisms and apoptotic pathways by which anthracycline influences cardiac structure and function. Anthracycline-induced apoptosis provides a very valid representation of cardiotoxicity in the heart, an argument which has implications for the most appropriate animal models of damaged heart plus diverse pharmacological effects. In this review we describe various aspects of the current understanding of apoptotic cell death triggered by anthracycline. Differences in the sensitivity to anthracycline-induced apoptosis between young and adult hearts are also discussed.
Authors:
Jianjian Shi; Eltyeb Abdelwahid; Lei Wei
Publication Detail:
Type:  JOURNAL ARTICLE    
Journal Detail:
Title:  Current pediatric reviews     Volume:  7     ISSN:  1875-6336     ISO Abbreviation:  -     Publication Date:  2011 Nov 
Date Detail:
Created Date:  2012-1-3     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101240290     Medline TA:  Curr Pediatr Rev     Country:  -    
Other Details:
Languages:  ENG     Pagination:  329-336     Citation Subset:  -    
Affiliation:
Riley Heart Research Center, Wells Center for Pediatric Research, Department of Pediatrics Indiana University, School of Medicine, Indianapolis, Indiana, USA.
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MeSH Terms
Descriptor/Qualifier:
Grant Support
ID/Acronym/Agency:
P01 HL085098-05//NHLBI NIH HHS

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