We have known for almost a century that mitochondria help us to turn food into usable energy by utilizing oxygen. We’ve known since 1938 that there are receptors in the carotid artery that signal to the brain when oxygen is low, directing faster breathing. We know that the body can create hormones like erythropoietin (EPO) in response to low oxygen, creating new blood vessels the carry much-needed oxygen. When our bodies are low on oxygen, the kidneys release EPO, which prompts bone marrow to start making more red blood cells (The Nobel Prize, 2019).
However, this year’s joint Nobel Winners for Physiology or Medicine, William G. Kaelin Jr., Sir Peter J. Ratcliffe, and Gregg L. Semenza, have found that many of the cells in the body, not just kidney cells, contribute to levels of EPO. They have discovered a protein that binds to DNA and turns on the production of EPO, called HIF-1a (hypoxia-inducible factor). Furthermore, the researchers have discovered the mechanism by which our cells control the regulation of EPO. When oxygen is present, it binds to HIF-1a, which essentially tags it for degradation instead of traveling to the nucleus and creating EPO (The Nobel Prize, 2019).
This research is very exciting because of its widespread possibilities. Many people who have kidney disease end up simultaneously suffering from anemia due to a lack of EPO.
There are types of cancer cells that are being researched because they appear to depend on oxygen. They actually use the body’s machinery to create more blood vessels around themselves so that more oxygen can arrive on the scene (The Nobel Prize, 2019). Understanding the cells’ basic machinery in oxygen sensing is a big first step in finding a way to help these patients.
No comments:
Post a Comment