This recycling system involves a protein complex known as retromer and lysosomes, which serve as cellular recycling centers to eliminate damaged genetic material.

The study demonstrated that increasing the activity of the retromer complex, particularly the protein VPS35, enhances the elimination of damaged mtDNA and improves mitochondrial function.

Dr. Parisa Kakanj collaborated on this research, utilizing fruit flies (Drosophila) to confirm the results observed in human cells, showing quicker removal of damaged mtDNA.

By preventing the accumulation of faulty mtDNA, this mechanism helps maintain cellular health and potentially prevents various diseases.

Dr. Kakanj emphasized that these findings pave the way for developing therapeutic strategies for mitochondrial diseases and age-related conditions.

Understanding this mechanism could explain how mitochondrial damage triggers diseases like Parkinson's and Alzheimer's, further highlighting its significance.

Researchers from University Hospital Düsseldorf, HHU, University of Cologne, and CMMC collaborated to discover a protective and repair mechanism for mitochondria when mtDNA damage is detected.

A groundbreaking study published in Science Advances has revealed a new cellular pathway essential for mitochondrial health, which could lead to preventive therapies for diseases linked to mitochondrial damage.

Damage to mitochondrial DNA (mtDNA) is associated with serious conditions such as Parkinson's, Alzheimer's, ALS, cardiovascular diseases, and type 2 diabetes, and it accelerates aging.

The research team, led by Professor Pla-Martín, identified a specialized recycling system that cells activate in response to mtDNA damage.

This collaborative research underscores the importance of interdisciplinary efforts in advancing our understanding of mitochondrial health.