Getting rid of garbage
Newly discovered protein helps to "clean" aged mitochondria
Scientists from the Medical University of South Carolina (MUSC, USA) have discovered the protein P17/PERMIT, which is the key to the processing of aging mitochondria and may be a link between age-related diseases such as cancer and Alzheimer's disease, the portal reports EurekAlert!. The results of the study are published in the journal Science Advances (Oleinik et al., Mitochondrial protein import is regulated by p17/PERMIT to mediate lipid metabolism and cellular stress).
Mitochondria are the organelles of cells that work as engines. Using the oxygen we breathe, they oxidize organic compounds and burn "fuel" – the energy that is produced when these compounds decay. Over time, these engines wear out: cells are increasingly stressed, mitochondria are more likely to "leak" the energy they produce. Energy overloads oxygen in our cells, which leads to the formation of highly active oxygen radicals, which our body tries to purify with antioxidants.
A "hole" in the mitochondria through which energy seeps is bad news for the cell. In an effort to get rid of the broken part, ceramide, a molecule that is produced in response to stress and cell damage, sends a signal to trigger the "digestion" of old mitochondria. This destructive process is known as mitophagy. When an entire cell has too much damage and cannot be repaired, ceramide can launch a program to destroy it.
What is the role of the newly discovered P17/PERMIT protein in this process? The protein is turned on at the very first stage. In response to stress, the cell makes the enzyme CerS1 responsible for the production of ceramide. PERMIT binds to a newly created enzyme and drags it into the mitochondria. The enzyme can then produce ceramide in large quantities – exactly in the place where it is necessary to regulate the mitochondria.
By understanding the function of protein, scientists can find a new solution to fight diseases such as cancer and Alzheimer's disease. Cancer cells can become dependent on defective mitochondria and will be forced to feed their growth, ignoring the normal signals that would lead the mitochondria to self-destruction. Meanwhile, the accumulation of proteins, which contributes to the development of the pathology of Alzheimer's disease, can begin with an incorrect "cleaning" of damaged mitochondria.
By unraveling the secrets of "repairing" and destroying mitochondria, the MUSC team hopes one day to develop a therapeutic agent that will mimic ceramide signals, ensuring proper "cleaning" of damaged mitochondria.
"We are trying to understand the link between cancer and Alzheimer's disease, and this protein may be a link," said Besim Ogretmen, head of the study, speaking about the P17/PERMIT protein. – Our idea is that, without changing the protein itself, we can generate ceramides in mitochondria using targeted therapy. It would help treat cancer and solve the problems associated with Alzheimer's disease."
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