Don't lose heart - therapeutic value of apoptosis prevention in the treatment of cardiovascular disease

Reeve, Janice L. V.; Duffy, Angela M.; O'Brien, Timothy; Samali, Afshin

doi:10.1111/j.1582-4934.2005.tb00492.x

Cited by 113Cell death mechanisms and regulationCardiac Ischemia and ReperfusionCardiac Fibrosis and Remodeling

Don't lose heart - therapeutic value of apoptosis prevention in the treatment of cardiovascular disease

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Reeve, Janice L. V., Duffy, Angela M., O'Brien, Timothy, Samali, Afshin·2005·Journal of Cellular and Molecular Medicine

DOI 10.1111/j.1582-4934.2005.tb00492.xPMC PMC6741425

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Abstract

Cardiovascular disease is a leading cause of death worldwide. Loss of function or death of cardiomyocytes is a major contributing factor to these diseases. Cell death in conditions such as heart failure and myocardial infarction is associated with apoptosis. Apoptotic pathways have been well studied in non-myocytes and it is thought that similar pathways exist in cardiomyocytes. These pathways include death initiated by ligation of membrane-bound death receptors, release of pro-apoptotic factors from mitochondria or stress at the endoplasmic reticulum. The key regulators of apoptosis include inhibitors of caspases (IAPs), the Bcl-2 family of proteins, growth factors, stress proteins, calcium and oxidants. The highly organized and predictive nature of apoptotic signaling means it is amenable to manipulation. A thorough understanding of the apoptotic process would facilitate intervention at the most suitable points, alleviating myocardium decline and dysfunction. This review summarizes the mechanisms underlying apoptosis and the mediators/regulators involved in these signaling pathways. We also discuss how the potential therapeutic value of these molecules could be harnessed.

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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 [295]

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Alnemri ES. Mammalian cell death proteases: a family of highly conserved aspartate specific cysteine proteases. J Cell Biochem. 1997; 64: 33-42.

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Cardiac remodeling in obesity
Abel, E. D., Litwin, S. E., & Sweeney, G. (2008) · Physiological Reviews · doi:10.1152/physrev.00017.2007 · Cited by 736 · see citing works

Authors: Reeve, J. L. V., Duffy, A. M., O'Brien, T., & Samali, A.
Affiliations: Ollscoil na Gaillimhe – University of Galway (IE)
ORCID: Reeve, Janice L. V.
Venue: Journal of Cellular and Molecular Medicine
Publisher: Wiley
Published: 2005-07
Volume: 9
Issue: 3
Pages: 609-622
ISSN: 1582-1838 (ISSN-L)
1582-4934
DOI: 10.1111/j.1582-4934.2005.tb00492.x
PMC: PMC6741425
OpenAlex: W1982685027
Cited by: 113
References: 135
Citations by year: 2026: 1 · 2024: 2 · 2023: 4 · 2022: 3 · 2021: 1 · 2020: 7 · 2019: 3 · 2018: 2 · 2017: 2 · 2016: 2 · 2015: 3 · 2014: 7 · 2013: 5 · 2012: 3
FWCI: 0.99
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: doi.wiley.com/10.1002/tdm_license_1.1 (tdm, 3714 d)
Locations: Journal of Cellular and Molecular Medicine (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Arrow@dit (Dublin Institute of Technology) (submittedVersion)
ARAN (University of Galway Research Repository) (Ollscoil na Gaillimhe – University of Galway) (submittedVersion, cc-by-nc-nd)
Funders: European Commission
Higher Education Authority
Irish Research Council for Science, Engineering and Technology
Irish Research Council
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, cardiomyocyte death, cardiovascular disease, heart failure, myocardial infarction, death receptors, mitochondrial apoptosis, endoplasmic reticulum stress, Bcl-2 family proteins, IAP, caspases, apoptosis signaling, cardioprotection
MeSH terms: Animals, Cardiovascular Diseases, Heat-Shock Proteins, Humans, Models, Biological, Apoptosis, Proto-Oncogene Proteins c-bcl-2, Intracellular Signaling Peptides and Proteins, CASP8 and FADD-Like Apoptosis Regulating Protein, Caspase Inhibitors

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Don't lose heart - therapeutic value of apoptosis prevention in the treatment of cardiovascular disease

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