Literature DB >> 14717062

Ins and outs of apoptosis in cardiovascular diseases.

G L Russo1, M Russo.   

Abstract

AIM: Cardiovascular disease (CVD) is the term used to define a group of disorders of the heart and blood vessels. Apoptosis, also known as programmed cell death (PCD), is genetically programmed "cell suicide" that plays an essential role in physiological processes such as embryo development, synaptogenesis, tissue turnover and the negative selection of T-cells, as well as in many diseases, such as cancer, and autoimmune and neurodegenerative diseases. The aim of this paper is to review the most recent data concerning the role of apoptosis in CVD, concentrating on the key apoptotic pathways in cardiomyocytes that may represent potential targets for therapeutic interventions. DATA
SUMMARY: The function of apoptosis in regulating CVD has recently been extensively investigated as a possible mechanism explaining the pathophysiological significance of various forms of CVD. Despite the difficulties of studying apoptosis in cardiomyocytes, a large number of studies of cellular and animal models suggest that they have the main apoptotic pathways that are also active in other cell types. However, the role of apoptosis in human pathologies, such as heart failure, ischemic heart disease and cardiac hypertrophy is still controversial. We revised classical (TUNEL) and novel experimental approaches (knock-out and transgenic mice; high-throughput genomics and proteomics) to address the role of apoptosis in CVD, concentrating on potential targets for therapeutic intervention.
CONCLUSION: Knowledge of the basic mechanisms regulating apoptosis activation and inhibition in cardiomyocytes may have important clinical and therapeutic implications.

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Year:  2003        PMID: 14717062     DOI: 10.1016/s0939-4753(03)80034-0

Source DB:  PubMed          Journal:  Nutr Metab Cardiovasc Dis        ISSN: 0939-4753            Impact factor:   4.222


  3 in total

1.  Dilated cardiomyopathy in the nmd mouse: transgenic rescue and QTLs that improve cardiac function and survival.

Authors:  Terry P Maddatu; Sean M Garvey; David G Schroeder; Wiedong Zhang; Soh-Yule Kim; Anthony I Nicholson; Crystal J Davis; Gregory A Cox
Journal:  Hum Mol Genet       Date:  2005-09-20       Impact factor: 6.150

2.  Overlapping roles of pocket proteins in the myocardium are unmasked by germ line deletion of p130 plus heart-specific deletion of Rb.

Authors:  W R MacLellan; A Garcia; H Oh; P Frenkel; M C Jordan; K P Roos; M D Schneider
Journal:  Mol Cell Biol       Date:  2005-03       Impact factor: 4.272

3.  Alcohol dehydrogenase accentuates ethanol-induced myocardial dysfunction and mitochondrial damage in mice: role of mitochondrial death pathway.

Authors:  Rui Guo; Jun Ren
Journal:  PLoS One       Date:  2010-01-18       Impact factor: 3.240

  3 in total

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