ArticleJournal of the American Society of Nephrology : JASN2019
APOL1 Kidney Risk Variants Induce Cell Death
Article in Journal of the American Society of Nephrology : JASN, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed.
- Genetic screening in kidney transplant candidates.Clinical kidney journal · 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 risk variants induce metabolic reprogramming of podocytes in patient-derived kidney organoids.Stem cell reports · 2025Article
- Article
- Review
- G1 and G2 ApolipoproteinL1 modulate macrophage inflammation and lipid accumulation through the polyamine pathway.bioRxiv : the preprint server for biology · 2025Article
- Apolipoprotein-L1 G1 variant contributes to hydrocephalus but not to atherosclerosis in apolipoprotein-E knock-out mice.Clinical science (London, England : 1979) · 2025Article
- The APOL1 p.N264K variant is co-inherited with the G2 kidney disease risk variant through a proximity recombination event.G3 (Bethesda, Md.) · 2025Article
- Defining Risk in APOL1-Associated Kidney Disease: The Story is Evolving!American journal of kidney diseases : the official journal of the National Kidney Foundation · 2024Article
- Collapsing Glomerulopathy.Advances in kidney disease and health · 2024Review
- Interferon-γ induces combined pyroptotic angiopathy and APOL1 expression in human kidney disease.Cell reports · 2024Article
- Vascular damage in systemic lupus erythematosus.Nature reviews. Nephrology · 2024Review
- IFI16 Is Indispensable for Promoting HIF-1α-Mediated APOL1 Expression in Human Podocytes under Hypoxic Conditions.International journal of molecular sciences · 2024Article
- APOL1-mediated monovalent cation transport contributes to APOL1-mediated podocytopathy in kidney disease.The Journal of clinical investigation · 2024Article
- Regulated cell death in chronic kidney disease: current evidence and future clinical perspectives.Frontiers in cell and developmental biology · 2024Review
- A SNARE protective pool antagonizes APOL1 renal toxicity in Drosophila nephrocytes.Cell & bioscience · 2023Article
- Novel Therapies inKidney international reports · 2023Review
- Article
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7 authors.
Funding
Abstract
backgroundGenetic Variants in Apolipoprotein L1 (APOL1) are associated with large increases in CKD rates among African Americans. Experiments in cell and mouse models suggest that these risk-related polymorphisms are toxic gain-of-function variants that cause kidney dysfunction, following a recessive mode of inheritance. Recent data in trypanosomes and in human cells indicate that such variants may cause toxicity through their effects on mitochondria.
methodsTo examine the molecular mechanisms underlying
resultsWe found that the APOL1 G0 and risk variant proteins shared the same import pathway into the mitochondrial matrix. Once inside, G0 remained monomeric, whereas risk variant proteins were prone to forming higher-order oligomers. Both nonrisk G0 and risk variant proteins bound components of the mitochondrial permeability transition pore, but only risk variant proteins activated pore opening. Blocking mitochondrial import of APOL1 risk variants largely eliminated oligomer formation and also rescued toxicity.
conclusionsOur study illuminates important differences in the molecular behavior of APOL1 nonrisk and risk variants, and our observations suggest a mechanism that may explain the very different functional effects of these variants, despite the lack of consistently observed differences in trafficking patterns, intracellular localization, or binding partners. Variant-dependent differences in oligomerization pattern may underlie APOL1's recessive, gain-of-function biology.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.