Researchers discovered that in response to stress, cells producing lipids dump their lipid stores into the lungs and fail to mop up the excess. The excess lipids react with oxygen to create a form of fat that acts as an inflammatory signal; in some ways this response is similar to the events that initiate atherosclerosis, or plaque formation in blood vessels.

In the lungs, researchers showed that immune cells called macrophages, which normally survey the lung for debris, infection, or dying cells begin gobbling up the excess fat in the lungs. Loaded with this oxidized fat, the macrophages turned on a program that acts to help heal the wounded tissue, but as a consequence to this adaptive response leads to the development of fibrotic lung disease.