Key result
PP2A modulates cardiac calcium handling, and its abnormal expression and activity are causal factors in arrhythmia and heart failure.
This review highlights the critical role of PP2A in regulating cardiac calcium transients and its pathophysiological implications in heart failure and arrhythmias.
Hypothesis-generating for PP2A-targeted therapies in arrhythmia and heart failure; prospective trials needed before clinical adoption.
Calcium transient in cardiomyocytes is regulated by multiple protein kinases and phosphatases. PP2A is a major protein phosphatase in the heart modulating Ca(2+) handling through an array of ion channels, antiporters and pumps, etc. The assembly, localization/translocation, and substrate specificity of PP2A are controlled by different post-translational mechanisms, which in turn are linked to the activities of upstream signaling molecules. Abnormal PP2A expression and activities are associated with defective response to β-adrenergic stimulation and are indication and causal factors in arrhythmia and heart failure.
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Lei et al. (2015) conducted a review in Arrhythmia and heart failure. Protein phosphatase 2A (PP2A) was evaluated. PP2A modulates cardiac calcium handling, and its abnormal expression and activity are causal factors in arrhythmia and heart failure.
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