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Newly Discovered Cellular Recycling System Repairs Mitochondrial DNA and May Help Prevent Disease

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frankerkanol
Messages : 18
Enregistré le : 04 avr. 2025, 20:01

Newly Discovered Cellular Recycling System Repairs Mitochondrial DNA and May Help Prevent Disease

Message par frankerkanol »

Damage to mitochondrial DNA (mtDNA), the genetic material within the cell’s energy-producing mitochondria, is linked to a range of serious health conditions, including Parkinson’s disease, Alzheimer’s, amyotrophic lateral sclerosis (ALS), cardiovascular disease, and type 2 diabetes. Such damage also plays a key role in accelerating the aging process. Fortunately, cells possess built-in mechanisms to detect and respond to this damage.

Now, researchers from University Hospital Düsseldorf and Heinrich Heine University Düsseldorf (HHU), in collaboration with the University of Cologne and the Center for Molecular Medicine Cologne (CMMC), have identified a previously unknown cellular mechanism that helps repair and protect mitochondria from genetic damage.

Led by Professor Pla-Martín of HHU’s Institute of Biochemistry and Molecular Biology I, the research team discovered that cells activate a specialized recycling system in response to mitochondrial DNA damage. Their findings, published in Science Advances, reveal that this system relies on a protein complex called the retromer and lysosomes—organelles that act as the cell’s recycling centers, breaking down and eliminating damaged genetic material.

This process plays a crucial role in preventing the accumulation of defective mtDNA, helping maintain healthy cellular function and potentially reducing the risk of disease.

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“We’ve identified a new pathway that’s essential for maintaining mitochondrial health and the cell’s natural defense mechanisms,” said Professor Pla-Martín. “Understanding this process gives us insight into how mitochondrial damage contributes to diseases like Parkinson’s and Alzheimer’s, and it could be a starting point for developing new preventive treatments.”

Working closely with Dr. Parisa Kakanj, a cell biologist at the University of Cologne and member of the CEPLAS Cluster of Excellence, the researchers extended their findings using fruit flies (Drosophila) as a model organism. Their experiments showed that increasing the activity of the retromer complex—specifically the protein VPS35—leads to a faster clearance of damaged mitochondrial DNA and a noticeable improvement in mitochondrial function.

“Using Drosophila allowed us to validate our initial findings in human cells and observe clear enhancements in mitochondrial health,” said Dr. Kakanj. “This opens up promising possibilities for developing therapies to treat mitochondrial and age-related diseases.”

This discovery represents a significant step forward in understanding how cells manage mitochondrial damage and offers new hope for future treatments targeting a wide range of degenerative diseases and aging-related conditions.
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