ArticleFrontiers in cell and developmental biology2026
Single-cell transcriptomic characterization of a human MDS hematopoietic dataset and in vitro validation of apoptosis-related venetoclax resistance in human MDS-L cells.
Article in Frontiers in cell and developmental biology, 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: Myelodysplastic syndromes (MDS) are heterogeneous clonal hematopoietic disorders in which dysregulated apoptosis, oxidative stress, and adaptive survival signaling contribute to disease persistence and therapeutic resistance. Venetoclax (VEN) targets BCL-2-dependent survival, but resistance is frequently accompanied by compensatory survival programs. Whether ferroptosis-associated transcriptional states are dynamically remodeled during VEN treatment and participate in this adaptive phenotype remains incompletely understood. Methods: We analyzed two independent human MDS single-cell RNA-sequencing cohorts together with an Results: Single-cell analysis revealed marked heterogeneity of ferroptosis-associated transcriptional programs across MDS hematopoietic populations. Longitudinal trajectories in GSE241417 demonstrated nonuniform, treatment-stage- and cell-state-dependent remodeling of ferroptosis balance, inflammatory context, and survival-associated programs. The independent GSE180298 cohort reproduced major disease-associated ferroptosis-related transcriptional differences. In VEN-resistant MDS-L cells, Conclusion: This study reveals cell-state-dependent and temporally dynamic ferroptosis-associated remodeling in MDS and identifies a coordinated apoptosis-redox transcriptional program associated with VEN resistance. The integration of longitudinal single-cell analysis, independent single-cell validation, and targeted qRT-PCR supports ferroptosis-defense pathways as a biologically relevant component of VEN-resistant adaptation and provides a rationale for future combination strategies that address both apoptotic dependence and redox-state plasticity.
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