Researchers led by Dr. Quan Lu, associate professor of environmental genetics and pathophysiology at Harvard T.H. Chan School Public Health, recently published a study in the Proceedings of the National Academy of Sciences (PNAS) that sheds light on the process that allows cells to bounce back from periods of intense stress and return to a healthy state. The findings, Dr. Lu said, could lead to new drug targets for a range of ailments, including diabetes, cancers, and neurodegenerative disorders.
Many factors can inflict stress on a cell. One common scenario begins with the endoplasmic reticulum (ER), an organelle within a cell that acts like an assembly line, synthesizing and delivering essential proteins, including those that sit on the cell surface. Each protein the ER produces is folded in a specific shape and serves a precise role. But sometimes the system malfunctions, resulting in proteins that are misfolded and that clog up the ER’s production process. When that happens, various molecules in the cell sense something is amiss and sound a proverbial alarm bell, which triggers a stress response. (Think of a factory foreperson shutting down an assembly line to get everything back in order.)
When a cell’s stress response kicks in, one of two things will happen: The cell either works out the kinks in the system and gets up and running again, or it’s overwhelmed and self-destructs, a process scientists call apoptosis. To date, Dr. Lu said, scientists have largely focused their efforts on analyzing the cascade of events that leads to apoptosis. But far less attention has been paid to understanding what happens inside cells that survive the stress response and return to a fully functional state.Friday Letter Submission, Publish on July 12