Apoptosis in ischemic heart disease

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Abstract

Apoptosis plays an important role in the myocardial loss after acute myocardial infarction and participates in the process of subsequent left ventricular remodeling and development of symptomatic heart failure. Finding a sensitive apoptotic marker that would help in prognostic stratification of patients after acute myocardial infarction and offer new therapeutic strategies is thus of a great importance. Several studies suggest that tumor necrosis factor-related apoptosis inducing ligand (TRAIL) represents a very promising marker of prognosis in patients with acute myocardial infarction. This review article provides an overview of current knowledge on the role of apoptosis in ischemic heart disease and highlights potentially beneficial apoptotic markers in clinical practice.

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Thomas G. Cotter (2009)

In multicellular organisms, the total number of cells is a balance between the cell-generating effects of mitosis and cell death that is induced through apoptosis. A disruption of this delicate balance can lead to the development of cancer. This Timeline article focuses on how the field of apoptosis biology has developed in the context of its contribution to our understanding of cell death, or lack of it, in the development of malignant disease. It traces the course of research from key discoveries in fundamental biology to potential therapeutic applications.

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Programmed cell death (PCD) pathways, including apoptosis and regulated necrosis, are required for normal cell turnover and tissue homeostasis. Mis-regulation of PCD is increasingly implicated in aging and aging-related disease. During aging the cell turnover rate declines for several highly-mitotic tissues. Aging-associated disruptions in systemic and inter-cell signaling combined with cell-autonomous damage and mitochondrial malfunction result in increased PCD in some cell types, and decreased PCD in other cell types. Increased PCD during aging is implicated in immune system decline, skeletal muscle wasting (sarcopenia), loss of cells in the heart, and neurodegenerative disease. In contrast, cancer cells and senescent cells are resistant to PCD, enabling them to increase in abundance during aging. PCD pathways limit life span in fungi, but whether PCD pathways normally limit adult metazoan life span is not yet clear. PCD is regulated by a balance of negative and positive factors, including the mitochondria, which are particularly subject to aging-associated malfunction.

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Viruses and apoptosis.

Philip E. Branton, A Roulston, Richard C. Marcellus (1998)

Successful viral replication requires not only the efficient production and spread of progeny, but also evasion of host defense mechanisms that limit replication by killing infected cells. In addition to inducing immune and inflammatory responses, infection by most viruses triggers apoptosis or programmed cell death of the infected cell. This cell response often results as a compulsory or unavoidable by-product of the action of critical viral replicative functions. In addition, some viruses seem to use apoptosis as a mechanism of cell killing and virus spread. In both cases, successful replication relies on the ability of certain viral products to block or delay apoptosis until sufficient progeny have been produced. Such proteins target a variety of strategic points in the apoptotic pathway. In this review we summarize the great amount of recent information on viruses and apoptosis and offer insights into how this knowledge may be used for future research and novel therapies.

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Author and article information

Contributors

Elena Teringova: elena.teringova@gmail.com

Petr Tousek:

ORCID: http://orcid.org/0000-0002-2598-3635

00420 739 888 552 , tousek@email.cz

Journal

Journal ID (nlm-ta): J Transl Med

Journal ID (iso-abbrev): J Transl Med

Title: Journal of Translational Medicine

Publisher: BioMed Central (London )

ISSN (Electronic): 1479-5876

Publication date (Electronic): 1 May 2017

Publication date PMC-release: 1 May 2017

Publication date Collection: 2017

Volume: 15

Electronic Location Identifier: 87

Affiliations

ISNI 0000 0004 0611 1895, GRID grid.412819.7, Cardiocenter, Department of Cardiology, 3rd Faculty of Medicine, , Charles University and University Hospital Kralovske Vinohrady, ; Srobarova 50, 100 34 Prague 10, Czech Republic

Author information

Petr Tousek http://orcid.org/0000-0002-2598-3635

Article

Publisher ID: 1191

DOI: 10.1186/s12967-017-1191-y

PMC ID: 5412049

PubMed ID: 28460644

SO-VID: 9694124e-b72f-4a93-bca2-b9a3f56f0c03

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

History

Date received : 19 January 2017

Date accepted : 21 April 2017

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ScienceOpen disciplines: Medicine

Keywords: apoptosis,ischemic heart disease,outcome,heart failure

Data availability:

ScienceOpen disciplines: Medicine

Keywords: apoptosis, ischemic heart disease, outcome, heart failure

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Apoptosis in ischemic heart disease

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Cardiovascular Innovations and Applications

Most cited references 50

Apoptosis and cancer: the genesis of a research field.

Programmed cell death in aging.

Viruses and apoptosis.

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Cited by 86

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