ArticleFrontiers in genetics2026
BHLHE41-SLC7A11 transcriptional axis and chromatin remodeling signatures in osteogenic-lineage disulfidptosis-like stress in osteoporosis.
Article in Frontiers in genetics, 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: Osteoporosis (OP) is characterized by impaired bone homeostasis in which bone resorption exceeds bone formation. Disulfidptosis, a recently described disulfide stress-induced cell death program linked to cytoskeletal collapse, has been suggested to contribute to OP, yet its cell-type-specific relevance within the bone marrow mesenchymal stem cell (BM-MSC) osteogenic lineage-and the upstream upstream transcriptional and epigenetic programs shaping this stress response-remain unclear. Methods: This study integrated a peripheral blood monocyte microarray dataset (GSE56815; 20 OP vs. 20 controls) with single-cell RNA sequencing to characterize disulfidptosis-related programs in OP. OP-associated disulfidptosis genes and molecular subtypes were identified using co-expression and differential analyses. Disulfidptosis score and upstream regulators across bone marrow cell populations were inferred from single-cell data using regulon analysis with motif/cis-regulatory evidence. Chromatin remodeling-related gene modules in osteoblasts were additionally scored to assess epigenetic activation/repression programs and their association with BHLHE41. Results: Integrated WGCNA with gene-overlap screening pinpointed 17 OP-linked disulfidptosis signature genes, highlighted by a marked increase of SLC7A11, and unsupervised stratification separated OP into two molecular subtypes. Single-cell analyses showed that disulfidptosis score was enriched in the osteoblast-like subset of BM-MSCs, implicating osteoblasts as a major affected population. Network inference further nominated BHLHE41 as a potential upstream driver of SLC7A11 and connected its expression with a disulfidptosis-tolerant phenotype in OP-derived BM-MSCs. Chromatin remodeling pathway scoring indicated altered epigenetic state programs in OP osteoblasts, and SIRT1 was preferentially upregulated in BHLHE41-high osteoblasts. Conclusion: This study provides a cell-type-resolved map of disulfidptosis-related stress in osteoporosis by integrating bulk and single-cell transcriptomics. We propose a BM-MSC osteogenic-lineage-associated BHLHE41-SLC7A11 axis and link it to chromatin remodeling signatures in osteoblasts, offering a rationale for precision strategies targeting disulfide-stress vulnerability in OP.
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