Atrial Transcriptional Profiles of Molecular Targets Mediating Electrophysiological Function in Aging and Pgc-1 β Deficient Murine Hearts
Conclusion: These findings limit the possible roles of gene transcriptional changes in previously reported age-dependent pro-arrhythmic electrophysiologial changes observed in Pgc-1β-/- atria to an altered Ca2+-ATPase (Atp2a2) expression. This directly parallels previously reported arrhythmic mechanism associated with p21-activated kinase type 1 deficiency. This could add to contributions from the direct physiological outcomes of mitochondrial dysfunction, whether through reactive oxygen species (ROS) production or altered Ca2+ homeostasis.
Introduction
Atrial arrhythmias constitute a major public health problem. Atrial fibrillation (AF), affects 1–3% of the developed world population. This prevalence will likely increase to ∼9 and ∼18 million cases in the United States and Europe, respectively, by 2060 (Miyasaka et al., 2006). Chronic AF increases incidences of both morbidity, often as stroke, and all-cause mortality.
Age is a major risk factor for AF, affecting 0.1, 4, and 20% of individuals aged <55, 60–70 and>80 years, respectively. So are metabolic factors, arising from physical inactivity, obesity, diabetes mellitus, and metabolic syndrome. Themselves age-dependent, these account for ∼60% of current upward trends in AF incidence (Miyasaka et al., 2006). Both age and metabolic deficiency in turn are associated with mitochondrial dysfunction (Vianna et al., 2006). Age is associated with mitochondrial DNA damage and...
Source: Frontiers in Physiology - Category: Physiology Source Type: research
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