{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T02:04:20Z","timestamp":1789524260938,"version":"build-2803163510"},"reference-count":42,"publisher":"Springer Science and Business Media LLC","license":[{"start":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T00:00:00Z","timestamp":1789516800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"},{"start":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T00:00:00Z","timestamp":1789516800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["GeroScience"],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Clonal haematopoiesis (CH)\u00a0is driven by somatic mutations in haematopoietic stem cells that generate clonal populations detectable in peripheral blood and is present in 10\u201320% of individuals over the age of 65. Mutations in\n                    <jats:italic>DNMT3A<\/jats:italic>\n                    and\n                    <jats:italic>TET2<\/jats:italic>\n                    are the most common drivers and have been linked to inflammatory phenotypes and increased risk of haematologic and cardiovascular disease. However, the cell-intrinsic mechanisms connecting these mutations to inflammatory signalling remain incompletely understood. Because retrotransposable elements (RTEs) are epigenetically regulated and can activate innate immune pathways when derepressed, we hypothesised that RTE reactivation may represent a mutation-specific mechanism linking clonal haematopoiesis driver mutations to inflammatory pathways. We analysed RTE expression and clonal burden in peripheral blood mononuclear cell (PBMC) samples from 56 individuals with CH and 12 non-CH controls using integrated genomic and transcriptomic approaches, with complementary validation by TARGET-seq across haematopoietic lineages.  High variant allele frequency (VAF;\u00a0&gt;\u200910%)\n                    <jats:italic>DNMT3A<\/jats:italic>\n                    -mutant clones exhibited widespread derepression of RTEs, particularly LINE and LTR families, whereas\n                    <jats:italic>TET2<\/jats:italic>\n                    -mutant clones showed a trend towards reduced RTE expression relative to controls. Transcriptomic analyses revealed that\n                    <jats:italic>DNMT3A<\/jats:italic>\n                    high-variant allele frequency clones with elevated RTE expression were enriched for inflammatory signalling pathways, including TNF-\u03b1\/NF-\u03baB signalling, interferon responses, and senescence-associated signatures. In contrast,\n                    <jats:italic>TET2<\/jats:italic>\n                    -mutant clones lacked these RTE-associated inflammatory signatures and instead showed enrichment of oxidative phosphorylation, reactive oxygen species signalling, and a mechanistic target of rapamycin complex 1 pathway. These findings were reproduced in an independent cohort.  Collectively, our\u00a0results\u00a0highlight mutation-specific inflammatory mechanisms in clonal haematopoiesis and provide a foundation for future functional and preclinical studies to determine whether modulation of RTE activity can influence the inflammatory phenotype of DNMT3A-mutant CH and represent a potential therapeutic strategy.\n                  <\/jats:p>","DOI":"10.1007\/s11357-026-02510-6","type":"journal-article","created":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T02:00:02Z","timestamp":1789524002000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Retrotransposable element derepression distinguishes DNMT3A-mutant from TET2-mutant clonal haematopoiesis"],"prefix":"10.1007","author":[{"given":"Maroof","family":"Hasan","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sylvia","family":"Durandeau","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"I. 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The study was approved by the London\u2013Bloomsbury Research Ethics Committee (IRAS 253604; REC reference 10\/LO\/1464).","order":1,"name":"Ethics","label":"Ethics approval and consent to participate","group":{"name":"EthicsHeading","label":"Declarations"}},{"value":"Not applicable.","order":2,"name":"Ethics","label":"Consent for publication","group":{"name":"EthicsHeading","label":"Declarations"}},{"value":"MH, RNVS, JC and AKG are employees and\/or stakeholders in BMS. The other authors declare no competing interests.","order":3,"name":"Ethics","label":"Competing interests","group":{"name":"EthicsHeading","label":"Declarations"}}]}}