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Airway Smooth Muscle in Bronchial Tone, Inflammation, and Remodeling

Basic Knowledge to Clinical Relevance

¹ Department of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania; ² Department of Biomedical Science, Cornell University College of Veterinary Medicine, Ithaca, New York; ³ Department of Pharmacology, University of Nevada School of Medicine, Reno, Nevada; ⁴ Department of Pediatrics, University of Michigan, Ann Arbor, Michigan; ⁵ Division of Pulmonary and Critical Care Medicine, University of California, San Francisco, San Francisco, California; ⁶ Division of Therapeutics, University Hospital of Nottingham, Nottingham, United Kingdom; and ⁷ Division of Lung Diseases, National Heart, Lung, and Blood Institute, Bethesda, Maryland

Correspondence and requests for reprints should be addressed to Susan Banks-Schlegel, Ph.D., Airway Biology and Disease Program, Division of Lung Diseases, National Heart, Lung, and Blood Institute, Two Rockledge Center, Suite 10042, 6701 Rockledge Drive, MSC 7952, Bethesda, MD 20892-7952. E-mail: schleges{at}nih.gov

ABSTRACT

Airway smooth muscle (ASM) plays a pivotal role in modulating bronchomotor tone but also orchestrates and perpetuates airway inflammation and remodeling. Despite substantial research, there remain important unanswered questions. In 2006, the National Heart, Lung, and Blood Institute sponsored a workshop to define new directions in ASM biology. Important questions concerning the key functions of ASM include the following: Does developmental dysregulation of ASM function promote airway disease, what key signaling pathways in ASM evoke airway hyperresponsiveness in vivo, do alterations in ASM mass affect excitation–contraction coupling, and can ASM modulate airway inflammation and remodeling in a physiologically relevant manner? This workshop identified critical issues in ASM biology to delineate areas for scientific investigation in the identification of new therapeutic and diagnostic approaches in asthma, chronic obstructive pulmonary disease, and cystic fibrosis.

Key Words: myocyte • signal transduction • force generation • migration • remodeling

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