Cited by 765Cardiac Fibrosis and RemodelingCell death mechanisms and regulationCardiac Ischemia and Reperfusion

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A mechanistic role for cardiac myocyte apoptosis in heart failure

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Wencker, Detlef, Chandra, Madhulika, Nguyen, Khanh, Miao, Wenfeng, Garantziotis, Stavros, Factor, Stephen M., Shirani, Jamshid, Armstrong, Robert C., Kitsis, Richard N.·2003·Journal of Clinical Investigation

DOI 10.1172/jci17664PMC PMC155051

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Abstract

Heart failure is a common, lethal condition whose pathogenesis is poorly understood. Recent studies have identified low levels of myocyte apoptosis (80-250 myocytes per 10(5) nuclei) in failing human hearts. It remains unclear, however, whether this cell death is a coincidental finding, a protective process, or a causal component in pathogenesis. Using transgenic mice that express a conditionally active caspase exclusively in the myocardium, we demonstrate that very low levels of myocyte apoptosis (23 myocytes per 10(5) nuclei, compared with 1.5 myocytes per 10(5) nuclei in controls) are sufficient to cause a lethal, dilated cardiomyopathy. Interestingly, these levels are four- to tenfold lower than those observed in failing human hearts. Conversely, inhibition of cardiac myocyte death in this murine model largely prevents the development of cardiac dilation and contractile dysfunction, the hallmarks of heart failure. To our knowledge, these data provide the first direct evidence that myocyte apoptosis may be a causal mechanism of heart failure, and they suggest that inhibition of this cell death process may constitute the basis for novel therapies.

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Authors: Wencker, D., Chandra, M., Nguyen, K., Miao, W., Garantziotis, S., Factor, S. M., Shirani, J., Armstrong, R. C., & Kitsis, R. N.
Affiliations: Albert Einstein College of Medicine (US)
Yeshiva University (US)
Pfizer (United States) (US)
Corresponding author: Kitsis, Richard N.
ORCID: Wencker, Detlef
Garantziotis, Stavros
Shirani, Jamshid
Kitsis, Richard N.
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 2003-05-15
Volume: 111
Issue: 10
Pages: 1497-1504
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci17664
PMC: PMC155051
OpenAlex: W2002958873
Cited by: 765
References: 29
Citations by year: 2026: 12 · 2025: 15 · 2024: 27 · 2023: 18 · 2022: 31 · 2021: 18 · 2020: 31 · 2019: 23 · 2018: 28 · 2017: 32 · 2016: 35 · 2015: 28 · 2014: 45 · 2013: 30 · 2012: 42
FWCI: 32.18
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Ariad Pharmaceuticals
New York Academy of Medicine
National Institutes of Health
National Heart, Lung, and Blood Institute (R01-HL-61550, R01 HL-60665, R01HL061550, R01HL060665)
Topics: Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
Keywords: cardiomyocyte apoptosis, heart failure, dilated cardiomyopathy, caspases, transgenic mice, myocardial cell death, contractile dysfunction, heart failure pathogenesis
MeSH terms: Animals, Disease Models, Animal, Enzyme Activation, Heart Failure, Humans, Mice, Inbred C57BL, Mice, Transgenic, Myocardium, Organ Specificity, Recombinant Fusion Proteins, Tacrolimus, Apoptosis, Disease Progression, Transgenes, Dimerization, Caspases, Enzyme Activators, Tacrolimus Binding Proteins, Myocytes, Cardiac, Mice, Caspase 8, Caspase 9

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A mechanistic role for cardiac myocyte apoptosis in heart failure

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