Staying young at heart: autophagy and adaptation to cardiac aging.

Staying young at heart: autophagy and adaptation to cardiac aging.
复制标题

保持年轻:自噬和适应心脏衰老。

DOI:
10.1016/j.yjmcc.2015.11.006
复制
发表时间:
2016-06
影响因子:
5
通讯作者:
Gustafsson ÅB
Gustafsson ÅB
中科院分区:
医学2区
文献类型:
--
作者:
Leon LJ;Gustafsson ÅB

文献摘要

被引文献

相似文献

衰老是发生心血管疾病的主要危险因素。因此,有助于衰老的细胞过程是治疗干预的有吸引力的目标,可以延缓或预防与年龄有关的疾病的发展。在过去的十年中,我们对导致细胞和组织功能随年龄增长而下降的潜在机制的理解有了很大的进展。细胞衰老的典型特征包括活性氧水平增加、DNA损伤、功能失调的细胞器积累、氧化的蛋白质和脂质。这些都导致细胞正常生理功能的逐渐下降,并导致与年龄相关的疾病的发生。衰老过程的一个主要原因是细胞质量控制的逐渐丧失。自噬是一种重要的质量控制途径,是维持心脏稳态和适应应激所必需的。在许多衰老模型中观察到自噬的减少,并且有令人信服的证据表明,增强的自噬可以延缓衰老并延长寿命。增强自噬抵消了细胞中与年龄相关的蛋白质聚集体和受损细胞器的积累。在这篇综述中,我们讨论了自噬在维持心脏稳态中的功能作用,以及自噬的下降与心脏加速衰老的关系。我们还将评估正在研究的治疗方法,以保持健康的年轻心脏。
Aging is a predominant risk factor for developing cardiovascular disease. Therefore, the cellular processes that contributes to aging are attractive targets for therapeutic interventions that can delay or prevent the development of age-related diseases. Our understanding of the underlying mechanisms that contribute to the decline in cell and tissue functions with age has greatly advanced over the past decade. Classical hallmarks of aging cells include increased levels of reactive oxygen species, DNA damage, accumulation of dysfunctional organelles, oxidized proteins and lipids. These all contribute to a progressive decline in the normal physiological function of the cell and to the onset of age-related conditions. A major cause of the aging process is progressive loss of cellular quality control. Autophagy is an important quality control pathway and is necessary to maintain cardiac homeostasis and to adapt to stress. A reduction in autophagy has been observed in a number of aging models and there is compelling evidence that enhanced autophagy delays aging and extents life span. Enhancing autophagy counteracts age-associated accumulation of protein aggregates and damaged organelles in cells. In this review, we discuss the functional role of autophagy in maintaining homeostasis in the heart, and how a decline is associated with accelerated cardiac aging. We will also evaluate therapeutic approaches being researched in an effort to maintain a healthy young heart.