Key result
Dysregulated RyR2 and SERCA2a calcium cycling promotes arrhythmogenesis in the aged heart.
Why the study?
Aging of the heart increases the propensity for arrhythmias and sudden cardiac death, driven at the cellular level by perturbations in excitation-contraction coupling and calcium homeostasis.
Design
Review
Authors
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May inform arrhythmia prevention strategies in older adults; extends mechanistic data but remains hypothesis-generating pending trials.
Understanding the molecular mechanisms of calcium dysregulation in the aging heart highlights potential therapeutic targets, such as mitochondrial ROS scavenging, to reduce arrhythmia burden in the elderly.
Hamilton et al. (2019) conducted a review in Arrhythmogenesis in the aging heart. Altered intracellular calcium homeostasis was evaluated. Aberrant changes in intracellular calcium cycling via RyR2 and SERCa2a, driven by post-translational modifications and mitochondrial oxidative stress, contribute to arrhythmogenesis in the aged heart.
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