ArticleFrontiers in cardiovascular medicine2026
Ionizing radiation expands a p90RSK-activated patrolling monocyte subset: modulation by colchicine.
Article in Frontiers in cardiovascular medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Ionizing radiation (IR) is known to induce vascular injury and alter immune cell function, yet the molecular mechanisms driving these changes remain incompletely defined. In particular, the role of clonal hematopoiesis-associated proteins expression and stress-responsive signaling pathways in monocyte subsets has not been fully elucidated. Methods: Peripheral blood mononuclear cells (PBMCs) from a single healthy human donor were pre-treated with colchicine and exposed to 2 Gy IR. After 24 h, cells were analyzed using CyTOF with a comprehensive antibody panel targeting lineage markers, DNA damage response proteins, efferocytosis receptors, and clonal hematopoiesis of indeterminate potential (CHIP) associated proteins, including DNMT3A and TET2. Data were processed using the Astrolabe platform to annotate canonical immune subsets. Results: While IR did not alter the overall immune cell frequency, colchicine increased the relative abundance of myeloid and B cell populations. Within CD14 Conclusion: Colchicine counteracts IR-induced immune remodeling by selectively inhibiting the expansion of CD14
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