This week on Lifespan News, Brent Nally discusses a study that links the hallmark of telomere attrition with the development of fibrosis.
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 myofibroblasts, 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 CDKN2Agene, preventing its expression. This reduces expression of the senescence marker p16.
TERT also represses the ACTA2 gene, according to this research. ACTA2 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, YB-1. However, ACTA2 also affects YB-1 expression, creating a complex feedback loop between TERT, YB-1, and ACTA2.
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-senescence strategy may affect organ fibrosis as well.
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