Mitochondria in old age: How we can fight chronic inflammation!

Transparenz: Redaktionell erstellt und geprüft.
Veröffentlicht am

New study at the Max Planck Institute and CECAD at the University of Cologne sheds light on the role of mitochondrial DNA in inflammation in old age.

Neue Studie am Max-Planck-Institut und CECAD der Universität zu Köln beleuchtet Rolle mitochondrialer DNA bei Entzündungen im Alter.
New study at the Max Planck Institute and CECAD at the University of Cologne sheds light on the role of mitochondrial DNA in inflammation in old age.

Mitochondria in old age: How we can fight chronic inflammation!

Chronic inflammation presents an increasingly common challenge, particularly as we age. In a recent study by the Max Planck Institute for Biology of Aging, in Nature was published, crucial connections between mitochondrial DNA and inflammatory processes were revealed. The researchers identified an imbalance in nucleotides, the building blocks of DNA and RNA, as one of the main causes of these inflammatory reactions. In particular, mitochondrial DNA leakage from mitochondria has been recognized as a catalyst for inflammation.

Mitochondria, often referred to as the “powerhouses of cells,” not only provide energy in the form of adenosine triphosphate (ATP), but also play an essential role in regulating inflammation. They are found in all cells of the body and have their own DNA, which makes them unique in their function. A lack of DNA building blocks in the cell leads to unstable mitochondrial DNA, the incorrect expansion of which leads to an inflammatory reaction. This discovery opens up new therapeutic possibilities for alleviating age-related inflammation.

Mitochondrial dysfunction and inflammation

Researchers at the Max Planck Institute also looked at the mitochondrial protein YME1L, which is linked to the release of mitochondrial DNA. Their results show that in cells that operate without YME1L, an accelerated release of mitochondrial DNA and an associated increased immune response occurs. This indicates that a lack of DNA building blocks can cause reactions similar to those caused by bacterial or viral infections. The addition of DNA building blocks from outside could prevent these inflammatory reactions.

A companion mouse model highlighted the dangers of an overabundance of RNA building blocks, which can lead to an accelerated inflammatory response and even earlier death. These findings make it clear that mitochondria could play a key role in the aging process and in the development of diseases associated with chronic inflammation, such as cardiovascular diseases or neurodegenerative disorders.

Therapeutic approaches and future perspectives

There are already therapeutic approaches aimed at treating mitochondrial diseases. However, it remains unclear whether these therapies are also effective against age-related inflammation. However, researchers see the metabolism of DNA building blocks as a promising field for future treatments, as they could be involved in various inflammatory diseases. The connection between mitochondrial DNA and diseases such as Alzheimer's, rheumatoid arthritis, obesity and cancer could open up new avenues for therapeutic strategies.

In addition, the role of mitochondria as an immune regulator is being increasingly researched. They send out signals that trigger immune reactions, especially in the event of cell damage or infection. These signals include, among other things, mitochondrial DNA and reactive oxygen species, the regulation of which is crucial for health. The natural and therapeutic approaches that are already available include a targeted diet with antioxidant active ingredients and regular physical activity that support mitochondrial functions.

In conclusion, the current research results not only expand the understanding of the mechanisms of chronic inflammation, but also offer new hope for promising therapeutic options. Caring for mitochondria could make a crucial contribution to long-term health.