Cited by 138Cell death mechanisms and regulationCardiac Ischemia and ReperfusionCardiac Fibrosis and Remodeling

Unresolved Issues Regarding the Role of Apoptosis in the Pathogenesis of Ischemic Injury and Heart Failure

Elsässer, Albrecht, Suzuki, Keisuke, Schaper, Jutta·2000·Journal of Molecular and Cellular Cardiology

Abstract

Unlabelled Apoptosis is "suicidal" programmed cell death followed by necrosis, i.e. cellular degradation. This review presents a critical evaluation of the methods used for detection of apoptosis and on data regarding the role of apoptosis in ischemia and heart failure.Methods DNA laddering by electrophoresis and the TUNEL method in histology for the final stage of apoptosis, Annexin V labeling, evidence of caspase activation, cleavage of substrates, measurements of mitochondrial pro-apoptotic and anti-apoptotic factors (Bcl-2, Bax and others) and determination of the mitochondrial transitional pore potential. Much work has been carried out regarding the mechanism and the importance of apoptosis in ischemia and heart failure but many issues still remain unsolved: (1)Time needed for completion of apoptosis from stimulus to DNA fragmentation? (2)Importance of mitochondrial pathway considering the fact that cardiomyocytes contain the highest volume density of mitochondria of all mammalian cells (25% in humans, 37% in mice)? (3)Means of removal of dead cells, disconnection at the intercalated disc from neighbouring myocytes, time frame of this process? (4)Reversibility of apoptosis? (5)Differences between physiological (postnatal differentiation of the conduction system) v pathological apoptotic cell death? (6)Why do cells, under ischemic conditions, die by either apoptosis or oncosis? (7)Is apoptosis an epiphenomenon or a true cause of heart failure? (8)Quantification of the rate of apoptosis in different pathophysiological situations? Clarification of these unresolved issues will then allow an estimation of the importance of apoptosis in cardiac pathophysiology and, if necessary because the role of apoptosis has been established, the development of new therapeutic concepts.

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Registry

Crossref · 10.1006/jmcc.2000.1125

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114 of 114 references verified0 citation errors · 0 not checkable

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  • Myocyte apoptosis has been suggested to be an important etiological component of heart failure, particularly in the transition from compensatory remodeling to heart failure, although this concept has been somewhat contentious.

    “Myocyte apoptosis has been suggested to be an important etiological component of heart failure, particularly in the transition from compensatory remodeling to heart failure (112), although this concept has been somewhat contentious (95, 189, 295, 301).”

    From Cardiac remodeling in obesity (2008) · cites this paper as [95]

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Authors
Elsässer, A., Suzuki, K., & Schaper, J.
Affiliations
  • University of Freiburg (DE)
  • Max Planck Society (DE)
Corresponding author
Schaper, Jutta
Venue
Journal of Molecular and Cellular Cardiology
Publisher
Elsevier BV
Published
2000-05
Volume
32
Issue
5
Pages
711-724
ISSN
0022-2828 (ISSN-L)
OpenAlex
W2045946370
Cited by
138
References
114
Citations by year
2024: 1 · 2023: 3 · 2022: 3 · 2021: 1 · 2020: 2 · 2019: 1 · 2018: 2 · 2017: 3 · 2016: 2 · 2015: 2 · 2014: 4 · 2013: 3
FWCI
1.11
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Molecular and Cellular Cardiology (publishedVersion)
  • PubMed (publishedVersion)
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
apoptosis, myocardial ischemia, heart failure, cardiomyocyte death, mitochondrial apoptosis, Bcl-2 family proteins, caspase activation, DNA fragmentation, TUNEL, oncosis, apoptosis quantification
MeSH terms
Animals, Cardiac Output, Low, Humans, Myocardial Ischemia, Apoptosis, Mice

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