The cardiokine story unfolds: ischemic stress-induced protein secretion in the heart.

The cardiokine story unfolds: ischemic stress-induced protein secretion in the heart.
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DOI:
10.1016/j.molmed.2010.12.003
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发表时间:
2011-04
影响因子:
13.6
通讯作者:
Glembotski CC
Glembotski CC
中科院分区:
医学1区
文献类型:
--
作者:
Doroudgar S;Glembotski CC

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细胞间的通讯很大程度上依赖于分泌的蛋白质。心源性分泌蛋白或心肌因子是动态的。例如,缺血等应激会将健康心脏中的心肌因子库转移到心脏应激反应所需的心肌因子库。当缺血心脏的条件不利于大多数心肌因子的表达、折叠和分泌时,这种转变是如何发生的?心肌因子的分泌在缺血期间维持或增加可能是不寻常的,因为它们可以承受不利的条件。由于压力诱导的心肌因子可能影响心脏对潜在致命压力的反应,如缺血,识别它们并描述它们的功能将扩大我们对如何治愈受损心脏的理解。
Cell-cell communication is largely dependent upon secreted proteins. The repertoire of cardiac-derived secreted proteins, or cardiomyokines, is dynamic. For example, stresses, such as ischemia, shift the cardiomyokine repertoire from those in the healthy heart, to those required for the cardiac stress response. How can this shift occur when conditions in the ischemic heart are unfavorable for the expression, folding and secretion of most cardiomyokines? Perhaps cardiomyokines whose secretion is maintained or increased during ischemia are unusual, in that they can withstand the unfavorable conditions. Since the stress-induced cardiomyokines could impact how the heart responds to potentially lethal stresses, such as ischemia, identifying them and characterizing their functions will broaden our understanding of how to heal the damaged heart.
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