title: Myofibroblasts and inflammatory cells as players of cardiac fibrosis.
abstract: On myocardial infarction, many cells are injured or died owing to arterial occlusion. Intracellular molecules released from injured or dead cells initiate inflammatory responses that play important roles in cardiac remodeling including fibrosis. Fibrosis is an excess accumulation of extracellular collagen. Currently, drugs used to treat cardiac fibrosis are not commercially available. Myofibroblasts are responsible for the production and secretion of collagen. Infiltrating inflammatory cells interact with fibroblasts or other cells and promote myofibroblast formation. Inflammatory cells also modulate the activities of myofibroblasts. Regulation of collagen production is critical for modulating the progression of fibrosis. Hence, the manipulation of activities of inflammatory cells and myofibroblasts will provide promising therapeutic targets for treatment of cardiac fibrosis.
authors: Department of Pharmacology and Toxicology, Graduate School of Pharmaceutical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan. hikurose@phar.kyushu-u.ac.jp.
authors: Hitoshi
authors: H
authors: Kurose
authors: Department of Pharmacology, Faculty of Pharmacy, Mahidol University, Bangkok, 10400, Thailand.
authors: Supachoke
authors: S
authors: Mangmool
mesh_terms: D000818:Animals; D003094:Collagen / Q000276:immunology*; D005355:Fibrosis / Q000276:immunology / Q000473:pathology; D006801:Humans; D007962:Leukocytes / Q000276:immunology / Q000473:pathology; D009203:Myocardial Infarction / Q000276:immunology* / Q000473:pathology*; D058628:Myofibroblasts / Q000276:immunology* / Q000473:pathology*; D009504:Neutrophils / Q000276:immunology / Q000473:pathology
chemical_list: D003094:Collagen
keywords: Cardiac fibrosis; Inflammation; Myocardial infarction; Myofibroblasts; Signaling molecules