Malfunctions in mitochondria influence skeletal aging
- Date:
- April 24, 2025
- Source:
- University of Cologne
- Summary:
- New mechanisms discovered that show how development-dependent disruptions in mitochondrial function lead to premature skeletal aging.
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An interdisciplinary research team led by Professor Dr Bent Brachvogel has examined how mitochondria influence the premature ageing of the skeleton. Mitochondria are also referred to as the 'powerhouses of the cells' and they play a key role in the production of energy by way of cellular respiration. Researchers have discovered that a development-dependent, premature impairment of mitochondrial respiration is responsible for speeding up the process of skeletal ageing. The study was published under the title "Metabolic rewiring caused by mitochondrial dysfunction promotes mTORC1-dependent skeletal aging" in Science Advances.
The researchers undertook a specific in vivo analysis of the mitochondrial malfunction in the skeletal system using a mouse model. They were able to show that a development-dependent impairment of the mitochondrial cellular respiration in cartilage cells leads to long-term change in cell metabolism. As a result of this metabolic adaptation, the cells lose their ability to regenerate in the long term and die, so that ageing processes in the skeleton are accelerated.
According to Professor Dr Bent Brachvogel, the responsible last author of the study, "The fundamental processes identified here could establish the basis for new treatment strategies to influence cartilage degeneration and skeletal aging in the context of mitochondrial disorders at an early stage."
The study was conducted in connection with the FOR2722 Research Unit. The research unit is examining the role of the extracellular matrix in the musculoskeletal system, the part of connective tissue that lies in the space between cells. One area of focus is the development of chronic degenerative diseases within the musculoskeletal system.
The study was led by the experimental neonatology team at University Hospital Cologne. Also participating in the study were researchers from the CECAD Cluster of Excellence for Aging Research, the Max Planck Institute for Biology of Ageing and from the Faculties of Mathematics and Natural Sciences at the Universities of Cologne and Erlangen-Nürnberg.
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Materials provided by University of Cologne. Note: Content may be edited for style and length.
Journal Reference:
- Kristina Bubb, Julia Etich, Kristina Probst, Tanvi Parashar, Maximilian Schuetter, Frederik Dethloff, Susanna Reincke, Janica L. Nolte, Marcus Krüger, Ursula Schlötzer-Schrehard, Julian Nüchel, Constantinos Demetriades, Patrick Giavalisco, Jan Riemer, Bent Brachvogel. Metabolic rewiring caused by mitochondrial dysfunction promotes mTORC1-dependent skeletal aging. Science Advances, 2025; 11 (16) DOI: 10.1126/sciadv.ads1842
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