Humans have always been fascinated by the concept of immortality, with multitudes of stories emerging throughout time about an elusive fountain of youth or a potion seductively promising everlasting life. While these stories have persisted in our mythos for centuries, such potions of youth have not yet been made a reality. That may change with the recent discovery that dying mitochondria trigger aging.
Mitochondria are small, bean-shaped structures within our cells that produce energy for the rest of the cell. Often, a single cell is powered by thousands of mitochondria. In a recent study, researchers observed that pores form in the mitochondrial membrane when a cell grows old or sick, causing the mitochondrion to burst and leak its inner contents into the rest of the cell. They found that when most of the mitochondria in a cell burst at the same time, the cell died. When just a small portion burst, the cell lived but was significantly diminished in function, as if the cell itself had aged. The researchers then treated old mice with drugs to stop mitochondrial bursting, finding that this treatment significantly reduced age-related health issues such as elevated brain inflammation and low mobility, balance, and bone strength.
While the drugs tested in this study significantly reduced the effects of aging in mice, promising drug candidates in mice studies have not always translated to success in human clinical trials. Nonetheless, discovering the connection between mitochondria bursting and cellular aging is an important first step towards the development of a safe and effective treatment for human age-related health issues. We have spent many centuries weaving stories about immortality and dreaming of the day that we could live not only longer but also more healthily. Those dreams may soon become a reality with the development of our very own potion of youth.
This study was led by researchers at the Mayo Clinic, Newcastle University, and the University of Glasgow, with collaborators from other institutions. The lead authors Stella Victorelli, Hanna Salmonowicz, and James Chapman contributed equally to the study. Stephen W.G. Tait and João F. Passos are the corresponding authors.
Managing Correspondent: Jenny Kim
Press Article: Study Suggests a New Mechanism of Cellular Senescence (Lifespan.io)
Original Journal Article: Apoptotic stress causes mtDNA release during senescence and drives the SASP (Nature)
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