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EDITORIAL
In the first mini-review of this Highlighted Topics series, entitled "The first three minutes: smooth muscle contraction, cytoskeletal events, and soft glasses," S. Gunst and J. Fredberg discuss how contraction of the airway smooth muscle cell is the major effector of acute airway narrowing in asthma. This mini-review focuses on the evolution of the contractile event and the underlying changes in cytoskeletal molecules. In this mini-review, these changes are examined within a novel biophysical context. In particular, the novel hypothesis that the cytoskeleton of living cells behaves as a soft glassy material, in which case cytoskeletal proteins would be seen to modulate cell mechanical properties mainly by changing an effective temperature of the cytoskeletal matrix, is presented. The effective temperature, in turn, becomes an integrative empirical framework for studying protein interactions within the complex microenvironment of the cell body and, potentially, represents an easily quantified determinant of the ability of the cytoskeleton to deform, flow, and reorganize.
Also in this issue, in a mini-review entitled "Airway wall remodeling: friend or foe?," McParland et al. reveal how airway remodeling can be defined as changes in the composition, content, and organization of the cellular and molecular constituents of the airway wall. Although some of the changes associated with airway remodeling could protect the airways from exaggerated airway narrowing, it is more likely to be the basis for exaggerated airway narrowing in asthma patients. This mini-review addresses the possible mechanisms by which airway remodeling can contribute to airway hyperresponsiveness: 1) amplifying the effect of smooth muscle shortening, 2) increasing the ability of the airways to generate radial stress, 3) uncoupling of airway smooth muscle from parenchymal recoil, 4) reducing parallel elastance, 5) enhancing latch bridge formation, and 6) allowing airway smooth muscle adaptation to short length.
In the August issue, in a mini-review entitled "Do inflammatory mediators influence the contribution of airway smooth muscle contraction to airway hyperresponsiveness in asthma?," Fernandes et al. review how the loss of the bronchodilatory or bronchoprotective effects of a deep inhalation is a key feature of asthma pathophysiology. This mini-review discusses ways in which inflammatory mediators might contribute to this abnormality, and thus to airway constrictor hyperresponsiveness, in asthma. These investigators consider two mechanisms, 1) the increase in shortening velocity of airway smooth muscle and 2) the reduction of mechanical plasticity, as plausible mechanisms for the loss of deep inhalation-induced bronchodilation and delineate some possible molecular bases for these possible modes of dynamic contractile dysfunction.
Also in the August issue, in a mini-review entitled "Understanding airway pathophysiology by computed tomography," R. Brown and W. Mitzner explore how conventional measurements of lung function provide little insight into mechanisms underlying the pathology of asthma. A traditional measure of decreased expiratory flow could result from narrowed large airways, narrowed small airways, closed airways, altered elasticity, or regional heterogeneities in parenchyma or airways. To examine specific mechanisms and structural alterations in airways, a method such as high-resolution computed tomography (HRCT) is required to visualize airway size in vivo. HRCT allows the study of multiple individual airways during either contraction to closure or relaxation in real time, as well as changes in airway size with changes in lung volume. There are no other methods that can provide this kind of insight into airway behavior in vivo. In this mini-review, these investigators document the capabilities of HRCT by briefly reviewing highlights of experimental results from several canine and human studies.
In the September issue, in a mini-review entitled "Complexity of factors modulating airway narrowing in vivo: relevance to assessment of airway hyperresponsiveness," V. Brusasco and R. Pellegrino examine the complex interactions between factors favoring and opposing airway narrowing, thus modulating the bronchoconstrictor response to external stimuli in vivo. This mini-review is mainly focused on asthma, but mechanisms responsible for airway hyperresponsiveness in other diseases are also examined. The implications for practical assessment and interpretation of airway responsiveness data in clinical settings are also included.
As with other Highlighted Topics series of the Journal of Applied Physiology, the Associate Editors and I wish to provide a wide-angle view of a clinically relevant problem, which we firmly believe needs additional well-focused research. It is clear from the invited mini-reviews and the original papers of this series that the intimate mechanisms leading from cellular and molecular abnormalities to abnormal organ responses are far from being fully understood, but we hope that we have provided a strong framework for continuing research in this area. We remain committed to the ongoing publication of articles exploring airway hyperresponsiveness at the basic level as well as those articles that provide a translational or clinical perspective. Accordingly, we strongly encourage investigators working in this area to consider submitting their work to the Journal of Applied Physiology.
Journal of Applied Physiology
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