Scientists learn how cells manage to keep their mitochondria healthy

Cells are the building blocks of life, acting like tiny power stations that keep the body functioning. However, sometimes the DNA within parts of the cell known as mitochondria becomes damaged, which can lead to serious diseases.

Professor Pla-Martín from the Institute of Biochemistry and Molecular Biology at Heinrich-Heine University Düsseldorf is leading a research team that studies how cells remove or “recycle” damaged mitochondria.

In collaboration with cell biologist Dr. Parisa Kakanj from the University of Cologne, the researchers have gained new insights into cell recycling and repair mechanisms.

How mitochondria influence everyday life

Mitochondria are vital for survival because they turn food into fuel. Through a series of chemical reactions, mitochondria break down glucose into an energy molecule known as adenosine triphosphate (ATP), which powers all the body’s systems.

Mitochondrial DNA (mtDNA) is distinct from the cell’s nuclear DNA and is inherited exclusively from the mother. When mtDNA is damaged, it can cause heart disease, Alzheimer’s, type 2 diabetes, amyotrophic lateral sclerosis (ALS), and Parkinson’s.

Professor Pla-Martín’s research team has identified a specialized system that locates and recycles damaged mtDNA.

Cells recycle damaged mitochondria

The researchers focused on protein complexes called retromers. These cell parts contain digestive enzymes, which remove mutated genetic material. This reduction of faulty mtDNA results in greater cellular health. 

“We have identified a previously unknown cellular pathway, which is important for mitochondrial health and thus for the natural defenses of our cells. By understanding this mechanism, we can explain how mitochondrial damage can trigger diseases like Parkinson’s and Alzheimer’s,” said Professor Pla-Martín.

This discovery demonstrates that the body has a targeted way of dealing with flawed mtDNA instead of sacrificing whole mitochondria.

Why fruit flies matter

Early findings in human cells were supported by work in the Drosophila model. The fruit flies allowed researchers to observe how boosted levels of certain proteins accelerated the removal of defective gene fragments.

“Using Drosophila allowed us to confirm our initial findings in human cells and demonstrate clear improvements in mitochondrial health. This opens up exciting possibilities for therapeutic strategies for treating mitochondrial diseases and age-related conditions,” said Dr. Kakanj.

The results of these experiments demonstrate how clearing unwanted segments can restore balance and reduce the risk of health problems.

A window into age-related challenges

Cells can suffer mutations and damage more often as they age. Researchers now see that swift cleanup of damaged mitochondria might reduce the risk of conditions that frequently appear with advancing years.

This specialized clearance relies on key proteins that identify faulty spots, break them off, and direct them into compartments with enzymes. Clearing out faulty sections preserves the remainder and helps keep cells stable.

Youth, health, and damaged mitochondria

Experts note that focusing on smaller mitochondrial fragments spares the larger structure and saves energy. This targeted approach avoids a more significant crisis inside cells.

The research also sheds light on how specific therapies might someday target or enhance these cleanup processes. Knowing which molecules rev up the recycling system could lead to strategies that keep aging tissues healthier for longer.

Hope for medical advances

Each newly discovered step prompts more questions about preventing damage before it hits a tipping point. The retromer’s role in monitoring troublesome genetic spots encourages talk of future drugs that tap into nature’s existing tools.

Lab teams are investigating ways to control how quickly these power hubs respond when they sense errors. The ultimate goal is to reduce stress on vulnerable tissues, including brain regions that are sensitive to energy shortages.

Innovative solutions to limit cell damage

The results of the research suggest that harnessing this protective cellular mechanism may be an effective way to manage diseases without resorting to drastic interventions.

Small tweaks to cell maintenance might help the body handle damaged mitochondria before it piles up. If researchers can strengthen this pathway, better approaches to diagnosis, treatment, and even prevention could follow.

The experts remain optimistic about transforming these insights into practical solutions for patients.

The study is published in the journal Science Advances.

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