Synopsis of hypothetical mechanisms by which alveolarization-relevant genes related to the extracellular matrix (ECM) might be modulated by a sustained mechanical stretch induced by tracheal occlusion.

<p>Tissue stretch is transmitted to alveolar myofibroblasts directly by mechanoreceptors (integrins) and ion channels or indirectly by liberation of growth factors stored/secreted in the ECM. Subsequent activation of intracellular signalings leads to increased transcription of target genes linked to the ECM and involved in elastogenesis (tropoelastin, lysyl-oxidase, fibulin-5, integrins), cytoskeletal rearrangements and cell migration (integrins, drebrin1, tenascin-C), ECM remodeling (tissue inhibitor of matrix metalloproteinase-1, TIMP1) or cell proliferation (TIMP1).