ArticleBMC nephrology2020
APOL1 renal risk variants exacerbate podocyte injury by increasing inflammatory stress.
Article in BMC nephrology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 37 citations in OpenAlex.
- Impact of Apolipoprotein L1-Associated Pregnancy Complications on Kidney Disease Phenotypes in a HIV-Associated Nephropathy Mouse Model.Kidney360 · 2026Article
- APOL1 plasma membrane pools resist rapid protein degradation.Scientific reports · 2026Article
- The Role of APOL1 in Necrotizing Enterocolitis and Its Promise as a Diagnostic Biomarker.Mediators of inflammation · 2026Article
- APOL1-mediated kidney disease: a narrative review of the lessons learnt from the past 15 years.BMC nephrology · 2025Review
- Carrying APOL1 G1 allele is associated with cardiovascular complications during COVID-19 in an admixed population.Human genomics · 2025Article
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- Review
- Apolipoprotein-L1 G1 variant contributes to hydrocephalus but not to atherosclerosis in apolipoprotein-E knock-out mice.Clinical science (London, England : 1979) · 2025Article
- Review
- Protein-truncating variant in APOL3 increases chronic kidney disease risk in epistasis with APOL1 risk alleles.JCI insight · 2024Article
- Interferon-γ induces combined pyroptotic angiopathy and APOL1 expression in human kidney disease.Cell reports · 2024Article
- Normal and Dysregulated Sphingolipid Metabolism: Contributions to Podocyte Injury and Beyond.Cells · 2024Review
- Preeclampsia in mice carrying fetuses with APOL1 risk variants.bioRxiv : the preprint server for biology · 2024Article
- Apolipoprotein L1 (APOL1) renal risk variant-mediated podocyte cytotoxicity depends on African haplotype and surface expression.Scientific reports · 2024Article
- Characterization of immortalized human podocytes infected with lentivirus as anAmerican journal of clinical and experimental immunology · 2024Article
- APOL1-G2 accelerates nephrocyte cell death by inhibiting the autophagy pathway.Disease models & mechanisms · 2023Article
- A SNARE protective pool antagonizes APOL1 renal toxicity in Drosophila nephrocytes.Cell & bioscience · 2023Article
- APOL1 Induces Pyroptosis of Fibroblasts Through NLRP3/Caspase-1/GSDMD Signaling Pathway in Ulcerative Colitis.Journal of inflammation research · 2023Article
- Protective effects of budesonide on LPS-induced podocyte injury by modulating macrophage M1/M2 polarization: Evidence fromExperimental and therapeutic medicine · 2022Article
- Antisense oligonucleotides ameliorate kidney dysfunction in podocyte-specific APOL1 risk variant mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundApolipoprotein L1, APOL1, is a trypanosome lytic factor present in human and certain other primates. APOL1 gene variants, present in individuals of recent sub-Saharan African descent, increase risk for glomerular disease and associate with the disease progression, but the molecular mechanisms have not been defined.
objectivesWe focus on the mechanism how APOL1 variant proteins enhance podocyte injury in the stressed kidney.
methodsFirst, we investigated the expression of APOL1 protein isoform and the localization of APOL1 protein in the kidney. Next, we examined the role of APOL1 in the podocyte stress and the inflammatory signaling in the kidney after hemi-nephrectomy.
resultsWe identified a novel RNA variant that lacks a secretory pathway signal sequence and we found that the predicted APOL1-B3 protein isoform was expressed in human podocytes in vivo and by BAC-APOL1 transgenic mice. APOL1-B3-G2 transgenic mice, carrying a renal risk variant, manifested podocyte injury and increased pro-IL-1β mRNA in isolated glomeruli and increased IL-1β production in the remnant kidney after uninephrectomy. APOL1-B3 interacted with NLRP12, a key regulator of Toll-like receptor signaling.
conclusionsThese results suggest a possible mechanism for podocyte injury by which one of the APOL1 protein isoforms, APOL1-B3 and its renal risk variants, enhances inflammatory signaling.
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