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Demiray, A.

Publications and source records attributed to Demiray, A..

2 recordsLinked to original sources

Multi-Omics Integration Reveals Lipid Metabolic Reprogramming as a Driver of Cystogenesis in Autosomal Dominant Polycystic Kidney Disease (ADPKD)

Autosomal dominant polycystic kidney disease (ADPKD) is a most common hereditary kidney disorder and a major contributor to end-stage kidney disease (ESKD), but its molecular progression mechanisms are unclear. We performed metabolomic and transcriptomic profiling on a longitudinal cohort of 254 and 47 ADPKD patients, respectively, to identify molecular alterations and then applied Multi-Omics Factor Analysis (MOFA) to uncover coordinated signatures. Disease progression was associated with a marked shift in dysregulated lipids profile, increased acylcarnitines, and increased glycolytic metabolites, suggesting a shift from fatty acid oxidation (FAO) toward glycolysis. Transcriptomic analysis revealed enrichment of PPAR signaling, cytoskeletal remodeling, and cystogenesis, providing a mechanistic link between metabolic alterations and structural dysregulation. Integrative analysis identified a central axis where inflammation, metabolic reprogramming, and cytoskeletal remodeling converges. Our integrated multi-omics analysis defines a molecular framework where transcriptomic dysregulation drives metabolic reprogramming contribute to cystogenesis, providing potential biomarkers and insights to guide precision therapy in ADPKD progression. Lay SummaryThe clinical heterogeneity of ADPKD limits current prognostic tools for early disease progression, often delaying therapeutic intervention. This study integrates longitudinal clinical data with multi-omics profiling (whole-blood transcriptomics and plasma metabolomics) in a large ADPKD cohort using Multi-Omics Factor Analysis. This approach identified coordinated molecular signatures linking aberrant gene expression and metabolic reprogramming directly to disease progression, hypertension, and mortality status. These findings uncover novel mechanistic drivers of ADPKD and suggest biomarkers to enhance early risk stratification, supporting the development of precision medicine strategies.

bioinformatics↗

The role of iron uptake systems in the pathogenesis of colistin-resistant hypervirulent K. pneumoniae infections

Here we proposed the hypothesis that hypervirulent colistin resistant K.pneumoniae (ColR-Kp) exhibit high number of virulence factors and have enhanced survival capacity against neutrophil activity.\n\nWe studied virulence genes of ColR-Kp isolates and neutrophil response in 142 patients with invasive infections.\n\nThe patients infected with hypervirulent ST101 and ST395 ColR-Kp had higher 30-day mortality (58%, p=0.005 and 75%, p=0.003, respectively. The yersiniabactin biosynthesis gene (ybtS) and ferric uptake operon associated gene (kfu) were significantly higher in ST101 (99%, p=<0.001) and in ST395 (94%, p<0.012). Being in ICU (OR: 7.9; CI: 1.43-55.98; p=0.024), kfu (OR:27.0; CI:5.67-179.65; p<0.001) and ST101 (OR: 17.2; CI: 2.45-350.40; p=0.01) were found to be predictors of 30-day mortality. The uptake of kfu+-ybtS+ ColR-Kp by neutrophils was significantly higher than kfu--ybtS- ColR-Kp (78% vs 65%, p<0.001). However, kfu+-ybtS+ ColR-Kp were more resistant to the killing activity of neutrophils than negative ones (7.90 vs 4.22; p=0.001). The kfu+-ybtS+ ColR-Kp stimulated excessive NET formation while the NETs against kfu--ybtS- ColR-Kp were weak and rare.\n\nIron uptake systems enhance successful survival of K.pneumoniae against neutrophil phagocytic defense, and stimulate excessive NET formation. The drugs targeted to iron uptake systems would be a promising approach for treatment of hypervirulent K.pneumoniae infections.

microbiology↗