Increase in PKCα Activity during Heart Failure Despite the Stimulation of PKCα Braking Mechanism.

ABSTRACT: Rationale: Heart failure (HF) is marked by dampened cardiac contractility. A mild therapeutic target that improves contractile function without desensitizing the β-adrenergic system during HF may improve cardiac contractility and potentially survival. Inhibiting protein kinase C α (PKCα) activity may fit the criteria of a therapeutic target with milder systemic effects that still boosts contractility in HF patients. PKCα activity has been observed to increase during HF. This increase in PKCα activity is perplexing because it is also accompanied by up-regulation of a molecular braking mechanism. Objective: I aim to explore how PKCα activity can be increased and maintained during HF despite the presence of a molecular braking mechanism. Methods and Results: Using a computational approach, I

SUBMITTER: Aslam N 

PROVIDER: S-EPMC7177253 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature