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Damage to the mitochondria, the “power plants” of the cells, contributes to many diseases. Researchers from Heinrich Heine University Düsseldorf (HHU) and the University of Cologne led by HHU professor of medicine Dr David Pla-Martín, now describe in the scientific journal Science Advances how cells with defective mitochondria activate a special recycling system to eliminate damaged genetic material.

Damage to the genetic material of mitochondria – the mitochondrial DNA or mtDNA for short – can lead to diseases such as Parkinson’s, Alzheimer’s, amyotrophic lateral sclerosis (ALS), cardiovascular diseases and type 2 diabetes. Such damage also speeds up the ageing process. However, the cells are normally capable of identifying such damage and reacting.

Damage to the genetic material of mitochondria—the mitochondrial DNA or mtDNA for short—can lead to diseases such as Parkinson’s, Alzheimer’s, amyotrophic lateral sclerosis (ALS), cardiovascular diseases and type 2 diabetes. Such damage also speeds up the aging process. However, the cells are normally capable of identifying such damage and reacting.

Scientists from University Hospital Düsseldorf and HHU have—in collaboration with the University of Cologne and the Center for Molecular Medicine Cologne (CMMC)—discovered a mechanism which protects and repairs the mitochondria. The research team, headed by Professor Pla-Martín from the Institute of Biochemistry and Molecular Biology I at HHU, has identified a specialized recycling system, which cells activate when they identify damage to the mtDNA.

According to the authors in Science Advances, this mechanism relies on a known as retromer and the lysosomes—cell organelles containing digestive enzymes. These special cellular compartments act like recycling centers, eliminating the damaged genetic material.

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We live longer and longer, and as we age, a lot of us develop a series of health issues and chronic diseases, including Chronic Obstructive Pulmonary Disease (COPD), which is found in around 600 million individuals globally. However, only half of them know they have the disease.

COPD patients often experience shortness of breath, persistent cough with mucus, wheezing and frequent respiratory infections, which can make everyday activities difficult.

Now a new study from the University of Copenhagen and Bispebjerg Hospital suggests that a form of vitamin B3 may be the key to improving quality of life for these patients.

“In the study, we show that nicotinamide riboside, also known as vitamin B3, can reduce lung inflammation in COPD patients,” says Associate Professor Morten Scheibye-Knudsen from the Center for Healthy Aging at the Department of Cellular and Molecular Medicine, University of Copenhagen, who has co-authored the new study.


A new study carried out by researchers at the University of Copenhagen and Bispebjerg Hospital shows that a form of vitamin B3 can reduce lung inflammation in COPD patients.

In this Review, Della Valle et al. discuss the role of retrotransposable elements (RTEs) in the onset and progression of ageing and ageing-related disease, including evidence that environmental stressors act through RTEs to shift the trajectory towards unhealthy ageing.

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Japanese researchers are making groundbreaking discoveries on the mechanisms of aging and working to apply them. As we age, senescent cells, or aged cells that have stopped dividing, accumulate, causing inflammation that can damage blood vessels and organs. Animal experiments have shown that removing these cells improves kidney function and reduces arteriosclerosis. They have led to the identification of a drug and development of a vaccine to eliminate the cells.