Heart failure with preserved ejection fraction: Defining the function of ROS and NO

Li Zuo, Chia Chen Chuang, Benjamin T. Hemmelgarn, Thomas M. Best

Research output: Contribution to journalReview articlepeer-review

23 Scopus citations


The understanding of complex molecular mechanisms underlying heart failure (HF) is constantly under revision. Recent research has paid much attention to understanding the growing number of patients that exhibit HF symptoms yet have an ejection fraction similar to a normal phenotype. Termed heart failure with preserved ejection fraction (HFpEF), this novel hypothesis traces its roots to a proinflammatory state initiated in part by the existence of comorbidities that create a favorable environment for the production of reactive oxygen species (ROS). Triggering a cascade that involves reduced nitric oxide (NO) availability, elevated ROS levels in the coronary endothelium eventually contribute to hypertrophy and increased resting tension in cardiomyocytes. Improved understanding of the molecular pathways associated with HFpEF has led to studies that concentrate on reducing ROS production in the heart, boosting NO availability, and increasing exercise capacity for HFpEF patients. This review will explore the latest research into the role of ROS and NO in the progression of HFpEF, as well as discuss the encouraging results of numerous therapeutic studies.

Original languageEnglish (US)
Pages (from-to)944-951
Number of pages8
JournalJournal of applied physiology
Issue number8
StatePublished - Oct 15 2015
Externally publishedYes


  • Ejection fraction
  • Exercise
  • Heart failure with preserved ejection fraction
  • NADPH oxidases
  • Nitric oxide
  • Nitric oxide synthase
  • Reactive oxygen species
  • Superoxide

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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