Molecular mechanisms of cardioprotection by taurine on ischemia-induced apoptosis in cultured cardiomyocytes.
Molecular mechanisms of cardioprotection by taurine on ischemia-induced apoptosis in cultured cardiomyocytes.
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DOI:
10.1007/978-0-387-33504-9_28
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发表时间:
2006
影响因子:
--
通讯作者:
Kyoko Takahashi;T. Takatani;Y. Uozumi;Takashi Ito;T. Matsuda;Y. Fujio;S. Schaffer;J. Azuma
中科院分区:
文献类型:
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作者:
Kyoko Takahashi;T. Takatani;Y. Uozumi;Takashi Ito;T. Matsuda;Y. Fujio;S. Schaffer;J. Azuma
An integral part of the pathogenesis of heart failure is myocyte loss. The traditional explanation for myocyte loss was cell necrosis but there has been a surge of evidence affirming the role of apoptosis in the genesis of heart failure (Garg et al., 2005). Evidence for apoptotic cell death was shown in clinical cases of myocardial infarction, as well as in rabbit, rat, and mouse models of continuous ischemia or ischemia/reperfusion (Garg et al., 2005). It has been shown that the mitochondrial pathways participate in apoptosis induced by ischemia (Garg et al., 2005). Taurine (2-aminoethanesulfonic acid), the-amino acid, is one of the factors that regulates the degree of apoptosis during ischemia (Roysommuti et al., 2003; Schaffer et al., 2003). However, little is known about the cytoprotective signalling pathways mediate this response. We have previously reported that isolated neonatal cardiomyocytes become resistant to ischemia-induced apoptosis when exposed to medium containing 20 mM taurine (Takahashi et al., 2003). In this study, the interaction between taurine and mitochondria-mediated apoptosis is investigated in a newly developed simulated ischemia model utilizing isolated cardiomyocytes that are incubated with medium containing and lacking taurine and then sealed within cultured flasks (Takahashi et al., 2003, Takatani et al., 2004a, b).