Heidelberg researchers reveal secret of mitochondrial repair!

Heidelberg researchers reveal secret of mitochondrial repair!

The health of the human body is closely related to the functionality of the mitochondria, which are considered the “power plants” of the cells. A team of researchers from Heinrich Heine University Düsseldorf (HHU) and the University of Cologne have discovered a crucial mechanism that protects and repairs mitochondria. Their results, which were published in the renowned journal Science Advances, open up promising perspectives for the development of preventive therapies against serious diseases.

Damaged mitochondrial DNA (mtDNA) is important because it is linked to a variety of diseases, including Parkinson's, Alzheimer's, ALS, cardiovascular disease and type 2 diabetes. The researchers found that damage to mtDNA accelerates the aging process and threatens cellular health. An effective protective mechanism could therefore be crucial for the prevention of such diseases.

The mitochondrial repair mechanism

The scientists discovered a recycling system that is activated when mtDNA is damaged. This mechanism is based on a protein complex called retromer and lysosomes, which act as “recycling centers”. They eliminate damaged genetic material, helping to maintain cellular health. Prof. David Pla-Martín, one of the lead authors of the study, emphasizes that understanding this mechanism can contribute to the development of new therapies.

In their study, the researchers used the model organism Drosophila. It was shown that increased activity of the retromer complex, especially the protein VPS35, significantly improves mitochondrial function. The results from the experiments with Drosophila have now also been confirmed on human cells. This lays the foundation for possible therapeutic strategies to treat mitochondrial diseases and age-related conditions.

Connection with neurodegenerative diseases

In addition to the findings from HHU and the University of Cologne, further studies can shed light on the relevance of mtDNA in relation to neurodegenerative diseases. A recent study on Parkinson's disease examines the role of the IFNβ/IFNAR signaling pathways and their relationship to mtDNA. Here, dysregulated oxidative phosphorylation (OXPHOS) was identified as a major pathway in sporadic Parkinson's disease with dementia.

Researchers found that overproduction of reactive oxygen species (ROS) leads to oxidative mutations and damage to mtDNA. Loss of ND4 and ND5, subunits of the respiratory chain, were found in post-mortem brain samples from patients with severe Parkinson's disease. Animal models lacking IFNβ-IFNAR signaling show similarities to the diseases, with increased ROS levels and defective mitochondrial functions observed.

The study also describes how damaged mtDNA results in neurotoxicity. In vivo experiments in which mtDNA was injected into mice resulted in motor and cognitive impairments as well as neuronal loss. This highlights the far-reaching consequences that damaged mtDNA has on the brain, as it can cause neuronal damage in distant brain regions, including the olfactory bulbs.

In summary, the recent findings represent a promising step in research into mitochondrial diseases. The interplay between mtDNA damage and neurodegenerative diseases requires in-depth consideration. How hhu.de explains, the results of this research team may not only advance our understanding of diseases in the near future, but also support the development of new, targeted therapies. Provide further insight Nature, which address the specific signaling pathways in Parkinson's disease and highlight their importance for mitochondrial integrity.