Short telomeres - A hallmark of heritable cardiomyopathies.
Short telomeres - A hallmark of heritable cardiomyopathies.
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DOI：
10.1016/j.diff.2018.02.001
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发表时间：
2018-03
期刊：
影响因子：
--
通讯作者：
Blau HM
中科院分区：
文献类型：
--
作者：
Chang ACY;Blau HM
心血管疾病是全世界死亡的主要原因，发病率随着年龄的增长而增加。基因检测已经教会了我们很多关于驱动遗传性心肌病的致病途径。在这里，我们讨论了一个意想不到的联系缩短端粒，衰老的分子标志物，和遗传性心肌病。端粒位于染色体的末端，是DNA重复序列，在增殖组织中作为保护帽，随着每次细胞分裂而缩短。心肌细胞是一种异常，因为它们在出生后很大程度上是非增殖性的，并且在健康个体的一生中保持相对稳定的端粒长度。然而，越来越多的证据表明，在疾病状态下，心肌细胞端粒显著缩短。此外，这种缩短可能在线粒体功能障碍的发展中发挥积极作用，线粒体功能障碍是扩张性和肥厚性心肌病的病因学中心。阐明心脏中端粒-线粒体信号轴的机制将为我们对遗传性心肌病的理解提供新的见解，并可能导致识别以前未表征的治疗干预模式。
Cardiovascular diseases are the leading cause of death worldwide and the incidence increases with age. Genetic testing has taught us much about the pathogenic pathways that drive heritable cardiomyopathies. Here we discuss an unexpected link between shortened telomeres, a molecular marker of aging, and genetic cardiomyopathy. Positioned at the ends of chromosomes, telomeres are DNA repeats which serve as protective caps that shorten with each cell division in proliferative tissues. Cardiomyocytes are an anomaly, as they are largely non-proliferative post-birth and retain relatively stable telomere lengths throughout life in healthy individuals. However, there is mounting evidence that in disease states, cardiomyocyte telomeres significantly shorten. Moreover, this shortening may play an active role in the development of mitochondrial dysfunction central to the etiology of dilated and hypertrophic cardiomyopathies. Elucidation of the mechanisms that underlie the telomere-mitochondrial signaling axis in the heart will provide fresh insights into our understanding of genetic cardiomyopathies, and could lead to the identification of previously uncharacterized modes of therapeutic intervention.
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影响因子：
5.2
作者：
Cottage, Christopher T.;Neidig, Lauren;Sundararaman, Balaji;Din, Shabana;Joyo, Anya Y.;Bailey, Brandi;Gude, Natalie;Hariharan, Nirmala;Sussman, Mark A.
通讯作者：
Sussman, Mark A.
影响因子：
4.6
作者：
Hussain T;Saha D;Purohit G;Kar A;Kishore Mukherjee A;Sharma S;Sengupta S;Dhapola P;Maji B;Vedagopuram S;Horikoshi NT;Horikoshi N;Pandita RK;Bhattacharya S;Bajaj A;Riou JF;Pandita TK;Chowdhury S
通讯作者：
Chowdhury S
影响因子：
3.7
作者：
HAYFLICK, L;MOORHEAD, PS
通讯作者：
MOORHEAD, PS
DOI：
10.1073/pnas.1213294110
发表时间：
2013-04-09
影响因子：
11.1
作者：
Din, Shabana;Mason, Matthew;Sussman, Mark A.
通讯作者：
Sussman, Mark A.
影响因子：
64.8
作者：
Bassat E;Mutlak YE;Genzelinakh A;Shadrin IY;Baruch Umansky K;Yifa O;Kain D;Rajchman D;Leach J;Riabov Bassat D;Udi Y;Sarig R;Sagi I;Martin JF;Bursac N;Cohen S;Tzahor E
通讯作者：
Tzahor E