Scientists Dramatically Extend Human Cell Lifespan by Shortening DNA's Telomeres By Over the last two decades, scientists have honed in on some key causes of aging: ranging from DNA telomere length, DNA hyper methylation to mitochondrial DNA oxidation. And as scientists zero in on these structural changes to the human genome, the focus is shifting to how to fix them and reverse human aging. Last January for example, a research team at Stanford University School of Medicine figured out how to lengthen the telomeres in in human cells and increase their lifespan more than 10-fold. The telomeres are the celebrated clocks of life, squiggly candle wicks of non-coding nucleotides that shorten at the ends of our DNA, as cells reproduce over time. Human telomeres are made up of thousands of repeated nucleotides in a TTAGGG pattern and protect the chromosomal ends of DNA strands from fraying, much like a shoelace cap. They also protect the DNA from chromosomal misalignment during replication. The telomeres are protected themselves by six proteins called the shelterin complex. A shortening of the telomeres in certain cells has been associated with numerous diseases and cell dysfunction including aging, aplastic anemia, cancer, dyskeratosis congenita, Duchenne muscular dystrophy, hypertension, atherosclerosis and endothelial cell death. Critically, short telomeres also destabilize adult stem cell differentiation, essential for tissue regeneration throughout the body. This past January, in a study published in The Journal of the Federation of American Societies for Experimental Biology (FASEB), researchers at Stanford University's Baxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Institute for Stem Cell Biology and Regenerative Medicine and the Department of Mechanical Engineering, extended the telomere lengths of fetal lung fibroblast and 30 year old muscle myoblast cells by increasing their own production of a ribonucleoprot