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Protein sensor plays a role in lung fibrosis

Researchers at Weill Cornell Medicine have discovered a protein called SEL1L that plays a critical role in clearing collagen from tissue, and which may be a therapeutic target to help prevent fibrosis, scar tissue that interferes with organ function. The paper, published on Feb. 20 in Nature Communications, provides clues that could lead to drug development for diseases like lung fibrosis which have no therapeutic options currently.

The researchers discovered a mechanism that cells use to detect collagen production internally and regulate clearance of excess collagen in tissues.  The protein SEL1L acts as a sensor that responds to collagen production by triggering another protein called MRC2 which is involved in the uptake and disposal of collagen. This study suggests that a defective collagen clearing pathway based on MRC2 is a key part of the imbalance in fibrotic disease. The data show when SEL1L is overproduced in cells, it leads to increased MRC2 production and thereby prevents the accumulation of collagen. This pathway could eventually be therapeutically targeted to drive increased clearance of collagen to improve fibrosis when it is impaired. Next, Dr. Podolsky, who is also an attending physician at NewYork Presbyterian/Weill Cornell Medical Center, plans to investigate how SEL1L is impaired in fibrotic human lungs. The lab is also exploring the molecular consequences of when MRC2 is inadequately triggered in pulmonary fibrosis.

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