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1 Thoracic Diseases Research Unit, Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine and 2 Department of Physiology and Biophysics Mayo Clinic and Foundation, Rochester, Minnesota 55905
In this review, we examine the hypothesis that plasma membrane stress failure is a central event in the pathophysiology of injury from alveolar overdistension. This hypothesis leads us to consider alveolar micromechanics and specifically the mechanical interactions between lung matrix and alveolar epithelial cell cytoskeleton and plasma membrane. We then explore events that are central to the regulation of plasma membrane tension and detail the lipid-trafficking responses of in vitro deformed and/or injured cells. We conclude with a reference to upregulation of stress-responsive genes after membrane injury and resealing.
lipid trafficking; mechanical stress; lung injury; cell deformation
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