New research reveals that reduced protein mobility in chronic diseases could be driven by oxidative stress, providing opportunities for developing therapies to rescue protein mobility.
Cellular traffic congestion in chronic diseases suggests new therapeutic targets
Treating chronic disease has proven difficult because there is not one simple cause, like a single gene mutation, that a treatment could target. However, new research from MIT professor of biology and Whitehead Institute for Biomedical Research member Richard Young and colleagues reveals that many chronic diseases have a common denominator that could be driving their dysfunction: reduced protein mobility.
The researchers found that oxidative stress, caused by an increase in reactive oxygen species (ROS), is responsible for the reduced protein mobility. They treated cells with an antioxidant drug called N-acetyl cysteine and saw that this partially restored protein mobility.
This discovery provides opportunities to develop therapies to rescue protein mobility. The researchers are pursuing a variety of follow-ups, including the search for drugs that safely and efficiently reduce ROS and restore protein mobility.
