Why the study?
Does p38 MAP kinase inhibition or antioxidant therapy improve contractile function and reduce ROS formation in a rabbit model of pacing-induced heart failure?
Does p38 MAP kinase inhibition or antioxidant therapy improve contractile function and reduce ROS formation in a rabbit model of pacing-induced heart failure?
Answers are grounded in this paper and cite their sources.
In a rabbit model of heart failure, p38 MAP kinase activation acts upstream of ROS formation, and its inhibition improves contractile function and reduces myofibrillar oxidation.
No abstract yet. The journal hasn't published one we can show.
No takes yet. Share an insight, caveat, or question.
Heusch et al. (2010) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: