title: Molecular basis of diastolic dysfunction.
abstract: Diastolic dysfunction is characterized by prolonged relaxation, increased filling pressure, decreased contraction velocity, and reduced cardiac output. Phenotypical features of diastolic dysfunction can be observed at the level of the isolated myocyte. This article reviews the cellular mechanisms that control relaxation at the level of the myocyte in the healthy situation and discusses the alterations that can affect physiologic function during disease. It focuses specifically on the mechanisms that regulate intracellular calcium handling, and the response of the myofilaments to calcium, including the changes in these components that can contribute to diastolic dysfunction.
authors.affiliation: Davis Heart and Lung Research Institute, The Ohio State University, Columbus OH, USA. periasamy.1@osu.edu
authors.forename: Muthu
authors.initials: M
authors.lastname: Periasamy
authors.forename: Paul M L
authors.initials: PM
authors.lastname: Janssen
mesh_terms: D008841:Actin Cytoskeleton; D002118:Calcium / Q000502:physiology; D002302:Cardiac Output / Q000502:physiology*; D003971:Diastole; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D032342:Muscle Cells / Q000502:physiology*; D009119:Muscle Contraction; D009126:Muscle Relaxation; D009200:Myocardial Contraction; D009206:Myocardium; D012519:Sarcoplasmic Reticulum
chemical_list: D002118:Calcium