ArticleGenes2026
Drug Repositioning Based on Single-Cell Transcriptomics Data Identifies Quinidine as a Potential Drug for Treating Osteoporosis.
Article in Genes, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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10 authors.
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Abstract
Osteoporosis (OP) is characterized by low bone mass and impaired bone microarchitecture, and the long-term use of current therapies is limited by adverse effects and poor adherence. This study sought to identify drugs that could be repurposed for glucocorticoid-induced osteoporosis.
methodsSingle-cell RNA-sequencing data from two subjects with osteoporotic fractures and three control subjects were analyzed to identify transcriptional changes in osteoblasts. Candidate drugs were screened using ASGARD and L1000 drug-response signatures. Two-sample Mendelian randomization was used to examine associations between genetically predicted expression of drug-target genes and osteoporosis risk. Quinidine was tested in dexamethasone-treated Tu and Tg(
resultsFour candidate drugs were identified, of which quinidine was selected for experimental evaluation. Genetically predicted SCN5A expression was positively associated with osteoporosis risk. Quinidine partially restored cranial mineralization in dexamethasone-treated larvae, with the greatest effect at 10 μmol/L; the 100 μmol/L treatment was less effective. Quinidine also altered the expression of several bone-remodeling-related genes. In adult zebrafish, quinidine treatment was associated with higher bone mineral density and bone volume fraction than dexamethasone treatment alone.
conclusionsQuinidine alleviated several dexamethasone-induced skeletal phenotypes in zebrafish and represents a candidate for further drug-repurposing studies in osteoporosis. Direct validation of its molecular mechanism and safety profile is still required.
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