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首页> 外文期刊>Experimental Physiology >Keeping the clocks ticking as we age: changes in sinoatrial node gene expression and function in the ageing heart.
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Keeping the clocks ticking as we age: changes in sinoatrial node gene expression and function in the ageing heart.

机译:随着年龄的增长,时钟不断变化:心脏衰老时窦房结基因表达和功能的变化。

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摘要

The function of the sinoatrial node (SAN; the natural pacemaker of the heart) declines with age, leading to a condition called sick sinus syndrome, which is associated with a variety of cardiac arrhythmias or conduction disturbances (Dobrzynski et al. 2007). Sick sinus syndrome accounts for more than 50% of pacemaker implantations in people over 60 years of age. The decline in SAN function with age may occur as a result of structural changes (collagen deposition), alterations in ion channels (expression and/or function may be perturbed) and impairments in cell-to-cell communication (altered gap junction function). In this issue of Experimental Physiology, Tellez et al. (2011) have quantitatively characterized the expression of 86 mRNA transcripts (including ion channels, transporters, connexins and receptors) in the SAN and atrial myocardium from young (3 months) and aged (25 months) rats. Their data illustrate the enormous complexity of the ageing process in the heart.
机译:窦房结(SAN;心脏的自然起搏器)的功能会随着年龄的增长而下降,导致一种称为病态窦房结综合征的病状,与多种心脏心律不齐或传导障碍相关(Dobrzynski et al。2007)。在60岁以上的人群中,病态窦房结综合征占植入起搏器的50%以上。 SAN功能随年龄的下降可能是由于结构变化(胶原蛋白沉积),离子通道的变化(表达和/或功能可能受到干扰)以及细胞间通讯障碍(改变的缝隙连接功能)引起的。在本期《实验生理学》中,Tellez等人。 (2011)对来自幼鼠(3个月)和成年鼠(25个月)的SAN和心房心肌中86种mRNA转录物(包括离子通道,转运蛋白,连接蛋白和受体)的表达进行了定量表征。他们的数据说明了心脏衰老过程的巨大复杂性。

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