Road to the cure – from stem cells to new muscle

Road to the cure

What’s the best way to describe a researcher’s path in life science? “Road to the Cure” fits almost perfectly. Nearly every research topic in life science is connected to a disease, so whether you are working, for example, in cancer, neurodegenerative diseases or muscular dystrophy research, all that matters is that you are on the “Road to the Cure”.

It is not a coincidence that the street already exists in beautiful La Jolla, California, which is now the place of the largest concentrations of academic and biotechnology institutions in the world (1). The whole area attracts some of the most talented minds of our generation and includes many world-famous institutions, such as Sanford Burnham Prebys Medical Discovery Institute (SBP).

From muscle stem cells to new muscle 

Scientists at SBP have recently identified the mechanism that stops muscle cells from regenerating during aging (2). This knowledge could help slow down the decline in muscle mass and function that people experience as they get older, and more importantly, it could help patients suffering from muscular dystrophies, who experience a phenomenon of “accelerated aging” of their muscle tissues.

Usually muscle stem cells are resting and need to be activated to create new muscle fibers. In this resting state, muscle stem cells do not express MyoD, the key protein in muscle differentiation, until they have been activated to develop into a specific type of muscle. During aging, the human muscle stem cells transition to a permanently inactive state, meaning they become senescent and cannot be activated to form new muscle fibers. But what if there was a way to wake up senescent muscle stem cells, get them to replicate and advance through myogenesis – could it then be possible to help build muscle in patients that need it? While working on mouse models and human fibroblasts, the team at SBP discovered that old muscle stem cells spontaneously trigger a DNA damage response (DRR) that stops them from dividing, which is needed to form new muscle. The team were then able to develop new ways  to wake up senescent cells, initiate cell division and activate myogenesis. At the same time, they learnt the lesson that using old muscle stem cells to create new muscle led to the formation of myofibers with nuclear abnormalities. The study also showed the first evidence of DDR-mediated functional antagonism between senescence and MyoD-activated gene expression, and that cell cycle progression is required for the activation of the myogenic program – which brings us a step further along the “Road to the Cure”. And isn’t this what research is all about? Somewhere, something incredible is waiting to be discovered – we just need to find the right path to get there.

Skeletal muscle

Curious to discover more? Find our laboratory-verified assays for DNA Damage Signaling and Skeletal Muscle Myogenesis and Myopathy. Feel free to visit our Knowledge Center or take a look at our Pathway Analysis for a broad range of assay technologies dedicated to skeletal muscle research.



1. San Diego Business – Research Institutions (link)
2. Latela L. et al, DNA damage signaling mediates the functional antagonism between replicative senescence and terminal muscle differentiation, Genes Dev. 2017 Apr 1;31(7):648-659. doi: 10.1101/gad.293266.116. (link)

Laura Alina Mohr, M.Sc.

Laura Alina Mohr joined QIAGEN in 2015. She received her Master’s Degree in Chemical Biology at the Technical University Dortmund in Germany. During this time, she was involved in Systemic Cell Biology research at the prestigious Max Planck Institute. Before joining QIAGEN, Laura Alina worked at the Scripps Research Institute, San Diego, where she first focused on DNA damage/repair pathways and telomere biology. Later, she joined the Muscle Development, Aging and Regeneration program at the Sanford Burnham Prebys Medical Discovery Institute. At QIAGEN she is interested in gene expression profiling focusing on various biological pathways, e.g. cancer research and neurodegeneration.

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