Reduced Lancl1-As1 In Old Human Skeletal Muscle Diminishes Mitochondrial Activity, Shortens Mt-Mrna Poly(A) Tails, And Suppresses Myogenesis
As we age, our muscles naturally lose mass and function, a condition known as sarcopenia, which can lead to frailty and reduced independence. Scientists have been working to understand the underlying causes of this age-related muscle decline.
Recent research has shed light on a key player in this process: a type of genetic material called a long noncoding RNA, or lncRNA, specifically one named LANCL1-AS1. Researchers observed that levels of this particular lncRNA decrease significantly in aging human muscle. Interestingly, its levels increase robustly during the process of muscle regeneration.
The study revealed that LANCL1-AS1 works by forming a complex with a protein called LRPPRC. This partnership is crucial for maintaining the length of “poly(A) tails” on messenger RNAs (mRNAs) found within mitochondria, the energy-producing powerhouses of our cells. These poly(A) tails are vital for the stability and proper translation of mitochondrial mRNAs, which are essential for healthy mitochondrial function and energy production.
When LANCL1-AS1 levels are low, as seen in older muscle, these crucial poly(A) tails become shorter. This shortening leads to a decrease in mitochondrial activity and hinders the muscle’s ability to regenerate. The good news is that when researchers increased the levels of LANCL1-AS1 in muscle cells from older individuals and even in aged monkey muscle, they observed a restoration of mitochondrial activity and an improvement in muscle regeneration.
These findings suggest that maintaining or boosting the levels of this specific lncRNA could be a promising strategy to combat age-related muscle deterioration and improve overall muscle health as we get older.
Source: link to paper