Abstract
Systolic dysfunction in heart failure and diabetic cardiomyopathy is associated with diminished Ca2+ transient amplitude and impaired mitochondrial function due to reduced mito-[Ca2+], in parallel with increased emission of mitochondrial reactive oxygen species (mito-ROS). Restoration of mito-[Ca2+] in diseased myocytes as a therapeutic approach remains contentious, as facilitation of mito-Ca2+ uptake has been shown to both protect against and exacerbate stress-induced Ca2+ dependent arrhythmia.
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