Fibrosis and hypertrophy are central pathophysiological features of heart failure, contributing to impaired contractile and relaxing functions, as well as arrhythmia and death. Oxidative stress inhibits a critical cellular heart muscle cell pump called Na+-K+ ATPase, which regulates heart muscle contraction. Professor Gemma Figtree's team have engineered a mouse that is resistant to oxidative modification of this pump, preserving its function and found it to be resilient to heart muscle thickening and failure under conditions of extreme pressure load. This has led the team to hypothesize that targeting the Na+-K+ ATPase cellular pump will be a strong candidate for new therapeutic approaches. This is particularly relevant for patients with heart failure with preserved ejection fraction (HFpEF) who make up ~50% of heart failure population yet have no therapies that modify outcomes.
In this project Professor Gemma Figtree aims to investigate the potential of protecting the Na+-K+ pump as a therapeutic strategy for HFpEF. Positive findings may bring hope for patients with a huge unmet need.
Last updated04 April 2022