Deciphering STAT3 signaling in the heart: plasticity and vascular inflammation.

Deciphering STAT3 signaling in the heart: plasticity and vascular inflammation.
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DOI:
10.1111/j.1751-7133.2010.00175.x
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发表时间:
2010-09
期刊:
Congestive heart failure (Greenwich, Conn.)
影响因子:
--
通讯作者:
Booz GW
Booz GW
中科院分区:
其他
文献类型:
--
作者:
Kurdi M;Booz GW

文献摘要

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STAT3是一种转录因子,在心脏发育和保护中起着关键作用。在理解其分子化学方面的新进展揭示了STAT3在控制线粒体呼吸中的重要性,独立于其作为转录因子的功能,以及通过与其他转录因子和辅因子的相互作用调节炎症信号传导。本文的目的是双重的。首先,我们总结了最近对STAT3功能的一些见解。其次,我们试图说明出于治疗目的靶向特定细胞蛋白的复杂性,以及在试图破译心脏中特定信号通路的作用时考虑背景的必要性。在这种情况下,炎症、衰老、肥大和心力衰竭提供了新的环境,这些环境肯定会影响STAT3的功能以及与其激活相关的基因谱。
STAT3 is a transcription factor that plays a critical role in heart development and protection. New developments in understanding its molecular chemistry have revealed the importance of STAT3 in controlling mitochondrial respiration, independent of its function as a transcription factor, and in modulating inflammatory signaling through interactions with other transcription factors and co-factors. The purpose of this article is twofold. First, we summarize some recent insights into the function of STAT3. Second, we seek to illustrate the complexity of targeting a particular cellular protein for therapeutic purposes and the need to consider context when attempting to decipher the role of a particular signaling pathway in the heart. In this case, inflammation, aging, hypertrophy, and heart failure provide new environments that certainly impact on the functioning of STAT3 and on the gene profile linked to its activation.