'Dark genome' reveals different routes to inflammation in age-related condition
The study, published in GeroScience, investigated mutations in DNMT3A and TET2, the two most common mutations in clonal hematopoiesis, an age-related condition in which mutated blood stem cells expand and form larger populations of blood cells.
A recent study published in GeroScience delved into the genetic factors contributing to inflammation in clonal hematopoiesis, a condition prevalent in older adults. Researchers discovered that mutations in DNMT3A and TET2, the two most frequent mutations in this age-related condition, lead to different inflammatory pathways. Large DNMT3A-mutant clones exhibited widespread activation of normally suppressed retrotransposable elements, known as the dark genome, which includes ancient viral remnants.
This reactivation correlated with inflammatory processes such as TNF–NFκB and interferon signaling. Conversely, TET2-mutant clones showed reduced RTE activity and distinct changes in pathways related to cellular metabolism and oxidative stress, indicating alternative inflammatory mechanisms. Lead author Dr. Mohammad Mahdi Karimi emphasized the potential of these findings to identify new biomarkers for assessing risk and developing targeted treatments for diseases like cardiovascular issues and blood cancers.
Understanding these varied mechanisms could pave the way for innovative strategies to prevent or manage clonal hematopoiesis-related conditions.
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