Jeffrey B. Kopp

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.

The paper shows that calcineurin inhibition deactivates pyruvate dehydrogenase, leading to proximal tubule cell metabolic dysfunction and kidney fibrosis.

The paper investigates the role of APOL1 variants in cardiovascular and neurological diseases using mice, finding APOL1-G1 contributes to hydrocephalus but not atherosclerosis.

This study identifies β-III tubulin as a marker for anti-fibrotic pericytes in pulmonary fibrosis and shows that Tuj1-expressing pericytes release CXCL10 to inhibit pro-fibrotic macrophage differentiation.

The paper identifies CR1 variants as a risk factor for FSGS across diverse populations through a case-control study and variant analysis.

This study uses mouse models to show that fetal APOL1-G1 variants cause preeclampsia by inducing pro-inflammatory responses in placental and maternal monocyte cells.

The paper shows the APOL1 p.N264K variant reduces the risk of FSGS and kidney disease in individuals with G2 APOL1 risk alleles.

This study examines the association between HBA copy number and kidney disease risk in Black Americans, finding higher HBA copy number linked to increased CKD prevalence and ESKD incidence.

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

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.