**8. Conclusion**

Understanding the molecular mechanisms by which the ECM regulates smooth muscle cell function in disease remains a key challenge to developing effective therapeutics for managing tissue remodeling diseases such as obstructive lung and vascular diseases. Insight into the biology of the smooth muscle cell in these diseases has increased rapidly in the recent years, leading to the concept that successful strategies for managing tissue remodeling may include restoring smooth muscle phenotype. Such approaches could possibly involve modulating the ECM of the smooth muscle microenvironment, or the factors which are involved in the transmission of the biochemical and biomechanical properties of the ECM. Proteases of the coagulation and plasminogen activation systems are of particular interest as therapeutic targets, as they not only have roles in forming and modifying ECM, but also can directly stimulate changes in smooth muscle cell function and phenotype. The challenge is to target these proteases without disrupting their roles in hemostasis, in order to avoid bleeding complications.
