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Cited by 32Cell death mechanisms and regulationCardiac Ischemia and ReperfusionCardiac Fibrosis and Remodeling

Hypoxia-induced cleavage of caspase-3 and DFF45/ICAD in human failed cardiomyocytes

Todor, Anastassia, Sharov, Victor G., Tanhehco, Elaine J., Silverman, Norman, Bernabei, Alvise, Sabbah, Hani N.·2002·American Journal of Physiology-Heart and Circulatory Physiology
DOI 10.1152/ajpheart.01003.2001
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Abstract

It has been proposed that the hemodynamic deterioration associated with heart failure (HF) may be due in part to ongoing loss of viable cardiac myocytes through apoptosis. Hypoxia has been shown to promote apoptosis in normal cardiomyocytes. Adaptation and maladaptations inherent to heart failure can modify the susceptibility of cells to different stress factors. We hypothesized that HF modifies the threshold of cardiomyocytes to hypoxia-induced apoptosis. Cardiomyocytes were isolated from 18 human hearts explanted at the time of cardiac transplantation due to either ischemic cardiomyopathy (ICM) ( n = 9) or idiopathic dilated cardiomyopathy (IDC) ( n = 9). Tissue from five normal donor hearts (NL) for whom no suitable recipient was available was used as control. Cardiomyocytes were incubated for 3 h under normoxic (95% air-5% CO 2) or hypoxic (95% N 2-5% CO 2) conditions. Expression of caspase-3 and DNA fragmentation factor-45 (DFF45)/inhibitor of caspase-3-activated DNase (ICAD) was detected by Western blot analysis. Three hours of hypoxia did not affect the expression of these proteins in NL cardiomyocytes. In contrast, hypoxia led to cleavage of caspase-3 and DFF45/ICAD both in ICM and IDC. In conclusion, failing cardiomyocytes exhibit increased susceptibility to hypoxia-induced apoptosis.

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  • Endomyocardial biopsies from patients with dilated or ischemic cardiomyopathy and end-stage heart failure demonstrated apoptotic cardiomyocyte death, and there was increased susceptibility to hypoxia-induced apoptosis in cardiomyocytes isolated from failing human hearts.

    “Endomyocardial biopsies from patients with dilated or ischemic cardiomyopathy and end-stage heart failure demonstrated apoptotic cardiomyocyte death (253, 263), and there was increased susceptibility to hypoxia-induced apoptosis in cardiomyocytes isolated from failing human hearts (351).”

    From Cardiac remodeling in obesity (2008) · cites this paper as [351]

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Authors
Todor, A., Sharov, V. G., Tanhehco, E. J., Silverman, N., Bernabei, A., & Sabbah, H. N.
Affiliations
Henry Ford Health (US)
ORCID
Venue
American Journal of Physiology-Heart and Circulatory Physiology
Publisher
American Physiological Society
Published
2002-09-01
Volume
283
Issue
3
Pages
H990-H995
ISSN
  • 0363-6135 (ISSN-L)
  • 1522-1539
DOI
10.1152/ajpheart.01003.2001
OpenAlex
W2129753301
Cited by
32
References
40
Citations by year
2023: 1 · 2021: 1 · 2019: 1 · 2018: 1 · 2015: 3 · 2013: 2 · 2012: 1
FWCI
1.27
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Heart, Lung, and Blood Institute (HL49090-07, R01HL049090)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
Keywords
hypoxia, apoptosis, caspase-3, cardiomyocytes, heart failure, ischemic cardiomyopathy, dilated cardiomyopathy, DNA fragmentation
MeSH terms
Adult, Hypoxia, Cardiomyopathy, Dilated, Female, Heart Failure, Humans, Male, Middle Aged, Myocardium, Proteins, Myocardial Ischemia, Apoptosis, Muscle Fibers, Skeletal, Caspases, Apoptosis Regulatory Proteins, Caspase 3, In Vitro Techniques

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