ArticleNature medicine2017
Transgenic expression of human APOL1 risk variants in podocytes induces kidney disease in mice.
Article in Nature medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 212 papers, 3 of them syntheses that pooled it.
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Who cites it
212 citing papers in PubMed, 3 syntheses or guidelines pooled it, 345 citations in OpenAlex.
- Apolipoprotein L1 gene variants and kidney disease in patients with HIV: a systematic review and meta-analysis.Journal of nephrology · 2023Pooled it
- Phenome-wide association analysis suggests the APOL1 linked disease spectrum primarily drives kidney-specific pathways.Kidney international · 2020Pooled it
- Kidney disease in the setting of HIV infection: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference.Kidney international · 2018Guideline
- APOL1 kidney disease: a critical narrative review of molecular mechanisms, clinical heterogeneity, and the emerging therapeutic landscape.International urology and nephrology · 2026Review
- Matrix Gla Protein is a novel regulator of TGFβ-dependent fibroblast activation and kidney fibrosis.Molecular biomedicine · 2026Article
- APOL1 risk alleles modulate T cell receptor signaling to promote allograft rejection.The Journal of clinical investigation · 2026Article
- ELF3 links kidney function GWAS loci to maladaptive epithelial inflammation.Science advances · 2026Article
- APOL1 risk genotypes influence DNA methylation across multiple genomic elements in APOL1-APOL4- MYH9 region in African Americans.Clinical epigenetics · 2026Article
- Untargeted Plasma Proteomic Signatures and Late Graft Failure in Kidney Transplant Recipients.Transplantation · 2026Article
- Proteomic risk score for early prediction of kidney disease progression in individuals with APOL1 high-risk genotypes.Nature medicine · 2026Article
- Automatic Blood Protein Enrichment by Magnetic-COF Polymers.Analytical chemistry · 2026Article
- Identification of end-stage renal disease-associated loci in X chromosome: an X chromosome-wide association study.MedScience · 2026Article
- Germline-targeted baboon apolipoprotein L-1 protects mice against African trypanosomes.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Molecular Mechanisms of APOL1-Associated Kidney Disease.International journal of molecular sciences · 2026Review
- Article
- APOL1 plasma membrane pools resist rapid protein degradation.Scientific reports · 2026Article
- Emerging genetic mechanisms of glomerular proteinuria: a podocyte-centered multi-layer network perspective.Frontiers in genetics · 2026Review
- APOL1-mediated kidney disease: a narrative review of the lessons learnt from the past 15 years.BMC nephrology · 2025Review
- A novelRenal failure · 2025Article
- APOL1 kidney disease: conclusions from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference.Kidney international · 2025Article
152 more citing papers are in PubMed but not listed here.
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18 authors at 10 institutions in 2 countries.
Funding
Abstract
African Americans have a heightened risk of developing chronic and end-stage kidney disease, an association that is largely attributed to two common genetic variants, termed G1 and G2, in the APOL1 gene. Direct evidence demonstrating that these APOL1 risk alleles are pathogenic is still lacking because the APOL1 gene is present in only some primates and humans; thus it has been challenging to demonstrate experimental proof of causality of these risk alleles for renal disease. Here we generated mice with podocyte-specific inducible expression of the APOL1 reference allele (termed G0) or each of the risk-conferring alleles (G1 or G2). We show that mice with podocyte-specific expression of either APOL1 risk allele, but not of the G0 allele, develop functional (albuminuria and azotemia), structural (foot-process effacement and glomerulosclerosis) and molecular (gene-expression) changes that closely resemble human kidney disease. Disease development was cell-type specific and likely reversible, and the severity correlated with the level of expression of the risk allele. We further found that expression of the risk-variant APOL1 alleles interferes with endosomal trafficking and blocks autophagic flux, which ultimately leads to inflammatory-mediated podocyte death and glomerular scarring. In summary, this is the first demonstration that the expression of APOL1 risk alleles is causal for altered podocyte function and glomerular disease in vivo.
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