 Is there any link between telomere attrition and fibrosis? And if so, how would this link impact future research? Stick around to find out. Oh, and guys, if you're playing basketball, clip your fingernails, please. A new study published in aging shows a link between the development of myofibroblast, which are cells involved in fibrosis, and a gene responsible for telomere maintenance called telomerase reverse transcriptase, or TERT. The researchers found that TERT regulates the expression of two genes. It binds to the promoter of the CDK-N2A gene, preventing its expression. This reduces expression of the senescence marker P16. TERT also represses the ACTA-2 gene, according to this research. ACTA-2 encodes a smooth muscle actin, or ASMA, which is responsible for cells differentiating into myofibroblasts. TERT affects this gene by regulating a transcription factor that controls it, YB1. However, ACTA-2 also affects YB1 expression, creating a complex feedback loop between TERT, YB1, and ACTA-2. The researchers did not fully characterize the dynamics of this network, which awaits further research. While this research is clearly in its infancy, and we are only beginning to understand the biochemical relationships involved, it already has significant implications for aging research and the development of future therapies. A link between TERT and myofibroblasts means that any future treatment that affects TERT as part of an anti-senescent strategy may affect organ fibrosis as well.