title: The crossroads of inflammation, fibrosis, and arrhythmia following myocardial infarction.
abstract: Optimal healing of damaged tissue following myocardial infarction (MI) requires a coordinated cellular response that can be divided into three phases: inflammatory, proliferative/reparative, and maturation. The inflammatory phase, characterized by rapid influx of cytokines, chemokines, and immune cells, is critical to the removal of damaged tissue. The onset of the proliferative/reparative phase is marked by increased proliferation of myofibroblasts and secretion of collagen to replace dead tissue. Lastly, crosslinking of collagen fibers and apoptosis of immune cells marks the maturation phase. Excessive inflammation or fibrosis has been linked to increased incidence of arrhythmia and other MI-related pathologies. This review describes the roles of inflammation and fibrosis in arrhythmogenesis and prospective therapies for anti-arrhythmic treatment.
authors.affiliation: Department of Pharmacology, University of California Davis, School of Medicine, Davis, CA, USA.
authors.forename: Samantha D
authors.initials: SD
authors.lastname: Francis Stuart
authors.affiliation: Department of Pharmacology, University of California Davis, School of Medicine, Davis, CA, USA.
authors.forename: Nicole M
authors.initials: NM
authors.lastname: De Jesus
authors.affiliation: Mississippi Center for Heart Research, Department of Physiology and Biophysics, University of Mississippi Medical Center and Research Service, G.V. (Sonny) Montgomery Veterans Affairs Medical Center, Jackson, MS, USA.
authors.forename: Merry L
authors.initials: ML
authors.lastname: Lindsey
authors.affiliation: Department of Pharmacology, University of California Davis, School of Medicine, Davis, CA, USA. Electronic address: cripplinger@ucdavis.edu.
authors.forename: Crystal M
authors.initials: CM
authors.lastname: Ripplinger
mesh_terms: D000818:Animals; D001145:Arrhythmias, Cardiac / Q000150:complications / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D002118:Calcium / Q000378:metabolism; D005355:Fibrosis; D005786:Gene Expression Regulation; D006801:Humans; D007249:Inflammation; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D017136:Ion Transport; D020782:Matrix Metalloproteinases / Q000235:genetics / Q000378:metabolism; D009203:Myocardial Infarction / Q000150:complications / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D053583:Interleukin-1beta; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D020782:Matrix Metalloproteinases; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D002118:Calcium
keywords: Arrhythmia; Fibrosis; Inflammation; Myocardial infarction