Jonathan Himmelfarb

This study identifies altered thick ascending limb cells with UMOD retention as drivers of CKD using spatial proteomics and shows reducing UMOD retention attenuates CKD development.

This paper introduces STORM, a statistical framework for analyzing spatial patterns in multi-omics data, demonstrating reliable performance in detecting spatial structures and supporting study design decisions.

This study compares voclosporin and cyclosporine A in 3D kidney MPS, finding that voclosporin preserves mitochondrial function and reduces proteostatic stress compared to cyclosporine A.

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 identifies a bacterial pathway for p-cresol removal and demonstrates its potential for gut-based detoxification.

This study investigates how indole affects the degradation of p-cresol by Thauera aminoaromatica S2 in planktonic and hydrogel-encapsulated forms, showing enhanced growth with low indole but inhibited degradation in hydrogels.

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.

This study investigates OTA toxicity in human kidney cells, showing it causes mitochondrial dysfunction, oxidative stress, and reduced energy production, contributing to kidney disease.

The paper uses ontologies to integrate clinical, pathological, and molecular kidney data for precision medicine analysis.

The paper defines the chromatin landscape of healthy and injured kidney cells using multi-omics data, identifying regulatory elements and transcription factor networks involved in injury response.

The paper constructs a reference tissue atlas of the human kidney using multi-omics data to identify cell types, pathways, and genes across nephron segments and interstitium.

The paper uses genome-edited human kidney organoids and single-cell transcriptomics to study APOL1 risk variants' effects on kidney disease mechanisms.