|
|
||||||||
University of Pennsylvania School of Medicine
Philadelphia, Pennsylvania
University of Chicago
Chicago, Illinois
Airflow obstruction in asthma, chronic obstructive pulmonary disease, and cystic fibrosis contributes markedly to the morbidity and mortality of these diseases. Although the precise mechanisms promoting airway obstruction remain unclear, airway smooth muscle (ASM) shortening plays a central role, and administration of bronchodilators to relax ASM has been a mainstay of treatment. Beyond its role in regulating airway luminal caliber, ASM may also secrete substances that promote airway inflammation, remodeling, and fibrosis. In the past five years, new therapies directed toward eliminating ASM (such as bronchial thermoplasty) have been developed, and their limited but beneficial effects in asthma prove the principle that ASM is indeed a reasonable therapeutic target. The goal of this issue is to provide concise reviews of important areas related to ASM function in hopes of developing new therapeutic strategies for modulating myocyte function. We hope that the greater understanding of ASM function gained from these reviews will inspire our readers to develop new approaches to preventing airflow obstruction while decreasing the morbidity and mortality from these common diseases.
FOOTNOTES
Conflict of Interest Statement: R.A.P. does not have a financial relationship with a commercial entity that has an interest in the subject of this manuscript. J.S. has received honoraria from various pharmaceutical companies (Merck, Tanox, Critical Therapeutics, Genentech, Cytokinetics) for service on their Advisory Boards, and has pending research grant support of approximately $254,000 from AstraZeneca.
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |