Viji Nair

The paper generates disease-specific genetic effect maps on the blood transcriptome for five glomerular diseases using whole genome and transcriptome sequencing data from the CureGN cohort.

This study identifies a MEF2C transcription factor network that regulates endothelial cell proliferation in diabetic kidney disease and shows that SGLT2i treatment can reverse its dysregulation.

This study shows dapagliflozin reduces hypoxia-induced metabolic stress, cell death, and fibrosis in kidney organoids derived from human pluripotent stem cells.

The paper presents a multi-modal atlas of human kidney disease, identifying cellular and spatial mechanisms of injury resolution or failure and linking them to clinical outcomes.

The paper analyzes glomerular transcriptomes to show APOL1 risk variants affect parietal epithelial cells in nephrotic patients, linking gene expression patterns to disease outcomes.

This study identifies early glomerular changes and gene expression patterns in Alport syndrome, showing ER stress and four genes as key drivers of disease before proteinuria, and highlights potential therapeutic targets.

This study uses single-cell RNA sequencing to identify a mechanosensitive MRTF-SRF pathway in early diabetic nephropathy, validated in human datasets and ex vivo experiments.

The paper identifies differentially methylated loci in individuals with end-stage kidney disease due to diabetic kidney disease, linking them to key pathways and genes.

The paper identifies a transcriptional signature of glomerular disease using single-cell profiling of human kidney organoids and validates it in disease cohorts.

This study identifies 16 genome-wide significant loci associated with diabetic kidney disease, including a protective variant in the COL4A3 gene.

The paper identifies high-risk nephrotic syndrome patients through transcriptome analysis and develops non-invasive biomarkers to predict disease progression.

The paper identifies shared molecular pathways between ANCA-associated vasculitis and nephrotic syndrome, highlighting JAK-STAT signaling as a potential therapeutic target.

The paper identifies eQTLs in glomerular and tubulointerstitial kidney tissues from nephrotic syndrome patients, finds tissue-specific eQTLs, and integrates them with a GWAS to identify associated genes.