title: Heart failure with preserved ejection fraction: Defining the function of ROS and NO.
abstract: 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.
authors.affiliation: Radiologic Sciences and Respiratory Therapy Division, School of Health and Rehabilitation Sciences, The Ohio State University College of Medicine, The Ohio State University Wexner Medical Center, Columbus, Ohio; and zuo.4@osu.edu.
authors.forename: Li
authors.initials: L
authors.lastname: Zuo
authors.affiliation: Radiologic Sciences and Respiratory Therapy Division, School of Health and Rehabilitation Sciences, The Ohio State University College of Medicine, The Ohio State University Wexner Medical Center, Columbus, Ohio; and.
authors.forename: Chia-Chen
authors.initials: CC
authors.lastname: Chuang
authors.affiliation: Radiologic Sciences and Respiratory Therapy Division, School of Health and Rehabilitation Sciences, The Ohio State University College of Medicine, The Ohio State University Wexner Medical Center, Columbus, Ohio; and.
authors.forename: Benjamin T
authors.initials: BT
authors.lastname: Hemmelgarn
authors.affiliation: Division of Sports Medicine, Department of Family Medicine, Sports Health & Performance Institute, The Ohio State University Wexner Medical Center, Columbus, Ohio.
authors.forename: Thomas M
authors.initials: TM
authors.lastname: Best
mesh_terms: D006321:Heart / Q000503:physiopathology*; D006333:Heart Failure / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D009206:Myocardium / Q000378:metabolism*; D032383:Myocytes, Cardiac / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism*
chemical_list: D017382:Reactive Oxygen Species; D009569:Nitric Oxide
keywords: NADPH oxidases; ejection fraction; exercise; heart failure with preserved ejection fraction; nitric oxide; nitric oxide synthase; reactive oxygen species; superoxide