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Between A ROCK And A Hard Place: Fasudil May Treat Pulmonary Fibrosis

Pulmonary fibrosis is a scarring or thickening of the that causes shortness of breath, a dry cough, fatigue, chest discomfort, weight loss, a decrease in the ability of the to transmit oxygen to the blood stream, and, eventually, heart failure. Cells known as normally secrete materials that are required for wound healing; once the wound has closed, the cells disappear. In pulmonary fibrosis, the stick around, continuing to secrete wound healing factors that cause fibrosis in the .

In this issue of the Journal of Clinical Investigation, and colleagues at identified a mechanosensitive cellular signaling pathway in myofibroblasts that is activated by the hardening of tissue that has become fibrotic. Activation of this pathway promotes myofibroblast survival and prevents the normal disappearance of these cells after completion of wound healing. The pathway is dependent on a protein known as ROCK. Zhou and colleagues found that a drug that inhibits ROCK, fasudil, attenuates the pro-survival pathway and causes myofibroblasts to die. Further, fasudil treatment protected mice from injury-induced .

These studies suggest that ROCK inhibitors could be used to treat pulmonary fibrosis. In a companion Attending Physician article, of the University of California, San Francisco, discusses the feasibility of using ROCK inhibitors in a clinical setting.

TITLE: Inhibition of mechanosensitive signaling in myofibroblasts ameliorates experimental pulmonary fibrosis



Journal of Clinical Investigation