How mitochondria influence the premature ageing of the skeleton
An interdisciplinary research team led by Professor Dr Bent Brachvogel, Faculty of Medicine, University of Cologne, Clinic and Polyclinic for Paediatric and Adolescent Medicine, Experimental Neonatology and associated member at the CMMC Center for Molecular Medicine, has examined how mitochondria influence the premature ageing of the skeleton. Mitochondria are also referred to as ‘cell powerhouses’ 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 (DOI: 10.1126/sciadv.ads1842).
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 ageing 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 -. The development of chronic degenerative diseases within the musculoskeletal system represents a particular area of focus here.
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.
Original publication
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 and Bent Brachvogel, Metabolic rewiring caused by mitochondrial dysfunction promotes mTORC1-dependent skeletal aging. Sci. Adv.11, eads1842 (2025). https://www.science.org/doi/10.1126/sciadv.ads1842
Scientific contact
Professor Dr Bent Brachvogel
bent.brachvogel[at]uni-koeln.de
Further information
https://for2722.uni-koeln.de/
This message has been modified by the CMMC (K. Heber & D. Grosskopf-Kroiher) and is based on the text provided by the press and communications team of the University of Cologne (Jan Voelkel, original version here).