Khrapko Konstantin, Trayanova Natalia, Nattel Stanley
Department of Biology, Northeastern University, Boston, MA 02115, USA.
Department of Biomedical Engineering, Johns Hopkins University, Baltimore, MD 21205, USA.
Cell Metab. 2015 May 5;21(5):662-3. doi: 10.1016/j.cmet.2015.04.024.
In this issue, Baris et al. (2015) describe cardiac rhythm abnormalities in a mouse model of mitochondrial dysfunction in widely distributed cells of the aging human heart. How do a few metabolically challenged cells disrupt cardiac rhythm? We suggest that these cells provide "crystallization centers" for latent dysfunctional zones to allow arrhythmia emergence.
在本期杂志中，巴里斯等人（2015年）描述了衰老人类心脏广泛分布细胞中线粒体功能障碍小鼠模型中的心律失常情况。少数代谢受到挑战的细胞是如何扰乱心脏节律的呢？我们认为，这些细胞为潜在功能失调区域提供了“结晶中心”，从而使心律失常得以出现。
