Cited by 81Cardiac Ischemia and ReperfusionCell death mechanisms and regulationCardiac Fibrosis and Remodeling

Apoptosis in myocardial infarction

Open access
Rodríguez, Manuel, Lucchesi, Benedict R, Schaper, Jutta·2002·Annals of Medicine

Abstract

Apoptosis, one of the major forms of cell death, has been implicated in different cardiovascular diseases. In this paper we review many of the different studies that have been performed to address the occurrence of apoptotic cell death associated with myocardial infarction. A definitive differentiation between apoptosis and other forms of cell death is still needed, mainly because of differences and limitations of the methods used for detection. In myocardial infarction apoptosis has been reported at acute stages of evolution in the ischemic area as well as in remote zones. In the ischemic area it might be a determinant of the final size of the infarct and it seems to depend on the presence of post-ischemic reperfusion. However, the incidence of apoptosis reported until now varies widely. In the myocardium remote from the ischemic area it might be associated with the progression towards heart failure. At present, the role and significance of apoptosis in myocardial infarction is rather inconclusive. Further studies are needed to solve methodological uncertainties and clarify the mechanisms involved in the process of cell death, which is particularly important as a basis for therapeutic interventions.

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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 [301]

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Research works printed but not linked: 2

  1. Vincenz C . Death receptors and apoposis. Cardiol Clin 2001; 19: 31±43.
  2. Takemura G, Kato S, Aoyama T, Hayakawa Y, Kanoh M, Maruyama R et al . Characterization of ultrastructure and its relation with DNA fragmentation in Fas-induced apoptosis of cultured cardiac myocytes. J Pathol 2001; 193: 546±56.

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Authors
Rodríguez, M., Lucchesi, B. R., & Schaper, J.
Affiliations
Max Planck Society (DE)
Venue
Annals of Medicine
Published
2002-01
Volume
34
Issue
6
Pages
470-479
ISSN
  • 0785-3890 (ISSN-L)
  • 1365-2060
OpenAlex
W2116040786
Cited by
81
References
85
Citations by year
2026: 3 · 2025: 3 · 2024: 4 · 2023: 2 · 2022: 6 · 2021: 2 · 2020: 3 · 2019: 2 · 2018: 2 · 2017: 1 · 2016: 1 · 2014: 3 · 2013: 6
FWCI
3.15
Type
journal article
Language
en
Open access
Locations
  • Annals of Medicine (publishedVersion)
  • PubMed (publishedVersion)
  • Max Planck Institute for Plasma Physics (submittedVersion)
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
Keywords
apoptosis, myocardial infarction, cell death, myocardial ischemia, ischemia-reperfusion injury, infarct size, heart failure, apoptosis detection methods
MeSH terms
Animals, Humans, Mitochondria, Myocardial Infarction, Myocardium, Tumor Suppressor Protein p53, Myocardial Ischemia, Apoptosis, Caspases, In Situ Nick-End Labeling, Myocytes, Cardiac, DNA Fragmentation

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