Health & Medicine
Cells 'Eat' Their Power Plants: Major Implications for Therapeutic Treatments with Mitochondria
Catherine Griffin
First Posted: Oct 01, 2013 08:54 AM EDT
Learning more about cells is crucial for creating better treatments for patients. Now, scientists have solved the mystery of a basic cellular process. It turns out that cells essentially "eat" their own power plants, the mitochondria, when they're damaged.
In order to learn a bit more about cellular processes, the researchers examined the mitochondria. One of the inner components of mitochondria are cardiolipins, named because they were first found in heart tissue. When a mitochondrioin is damaged, the cariolipins move from its inner membrane to its out membrane, where they encourage the cell to destroy the entire mitochondrion.
"It's a survival process," said Valerian Kagan, one of the researchers, in a news release. "Cells activate to get rid of bad mitochondria and consolidate good mitochondria. If this process succeeds, then the good ones can proliferate and the cells thrive. It's a beautiful, efficient mechanism that we will seek to target and model in developing new drugs and treatments."
That's only part of the process, though. A part of a protein called LC3 binds to cariolipin. This causes a specialized structure to form around the mitochondrion to carry it to the digestive centers in the cell. This type of cell-eating could have major implications for the study of Parkinson's disease and other issues.
"There are many follow-up questions," said Charleen Chu, one of the researchers, in a news release. "What is the process that triggers cariolipin to move outside the mitochondria? How does this pathway fit in with other pathways that affect onset of diseases like Parkinson's? Interestingly, two familial Parkinson's disease genes also are linked to mitochondrial removal."
This process may happen in all cells with mitochondria, yet it's important that it functions correctly in neuronal cells. These cells in particular do not divide and regenerate as readily as cells in other parts of the body.
The findings could have huge implications for brain surgery patients. The mitochondrial "eat me" signaling process could be a therapeutic target in the sense that you need a certain level of clearance of damaged mitochondria. In the future, this research could help develop treatments and therapies for patients.
The findings are published in the journal Nature Cell Biology.
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First Posted: Oct 01, 2013 08:54 AM EDT
Learning more about cells is crucial for creating better treatments for patients. Now, scientists have solved the mystery of a basic cellular process. It turns out that cells essentially "eat" their own power plants, the mitochondria, when they're damaged.
In order to learn a bit more about cellular processes, the researchers examined the mitochondria. One of the inner components of mitochondria are cardiolipins, named because they were first found in heart tissue. When a mitochondrioin is damaged, the cariolipins move from its inner membrane to its out membrane, where they encourage the cell to destroy the entire mitochondrion.
"It's a survival process," said Valerian Kagan, one of the researchers, in a news release. "Cells activate to get rid of bad mitochondria and consolidate good mitochondria. If this process succeeds, then the good ones can proliferate and the cells thrive. It's a beautiful, efficient mechanism that we will seek to target and model in developing new drugs and treatments."
That's only part of the process, though. A part of a protein called LC3 binds to cariolipin. This causes a specialized structure to form around the mitochondrion to carry it to the digestive centers in the cell. This type of cell-eating could have major implications for the study of Parkinson's disease and other issues.
"There are many follow-up questions," said Charleen Chu, one of the researchers, in a news release. "What is the process that triggers cariolipin to move outside the mitochondria? How does this pathway fit in with other pathways that affect onset of diseases like Parkinson's? Interestingly, two familial Parkinson's disease genes also are linked to mitochondrial removal."
This process may happen in all cells with mitochondria, yet it's important that it functions correctly in neuronal cells. These cells in particular do not divide and regenerate as readily as cells in other parts of the body.
The findings could have huge implications for brain surgery patients. The mitochondrial "eat me" signaling process could be a therapeutic target in the sense that you need a certain level of clearance of damaged mitochondria. In the future, this research could help develop treatments and therapies for patients.
The findings are published in the journal Nature Cell Biology.
See Now: NASA's Juno Spacecraft's Rendezvous With Jupiter's Mammoth Cyclone