title: Modeling the aging heart: from local respiratory defects to global rhythm disturbances.
abstract: 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.
authors.affiliation: Department of Biology, Northeastern University, Boston, MA 02115, USA. Electronic address: k.khrapko@neu.edu.
authors.forename: Konstantin
authors.initials: K
authors.lastname: Khrapko
authors.affiliation: Department of Biomedical Engineering, Johns Hopkins University, Baltimore, MD 21205, USA. Electronic address: ntrayan1@jhu.edu.
authors.forename: Natalia
authors.initials: N
authors.lastname: Trayanova
authors.affiliation: Department of Medicine, Montreal Heart Institute and Université de Montréal, Montréal, QC H1T 1C8, Canada. Electronic address: stanley.nattel@icm-mhi.org.
authors.forename: Stanley
authors.initials: S
authors.lastname: Nattel
mesh_terms: D000375:Aging; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology*; D004272:DNA, Mitochondrial / Q000235:genetics*; D008928:Mitochondria / Q000235:genetics*; D028361:Mitochondrial Diseases / Q000150:complications* / Q000235:genetics*; D010100:Oxygen / Q000378:metabolism*
chemical_list: D004272:DNA, Mitochondrial; D010100:Oxygen