ArticlePloS one2019
APOL1-G0 protects podocytes in a mouse model of HIV-associated nephropathy.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 30 citations in OpenAlex.
- Impact of Apolipoprotein L1-Associated Pregnancy Complications on Kidney Disease Phenotypes in a HIV-Associated Nephropathy Mouse Model.Kidney360 · 2026Article
- Article
- Precision Diagnosis in APOL1 Kidney Disease With the p.N264K M1 Protective Variant.JAMA network open · 2026Article
- APOL1-mediated kidney disease: a narrative review of the lessons learnt from the past 15 years.BMC nephrology · 2025Review
- Review
- HIV-1 Nef synergizes with APOL1-G1 to induce nephrocyte cell death in HIV-related kidney diseases.Disease models & mechanisms · 2025Article
- Pathogenesis of HIV-associated nephropathy in children and adolescents: taking a hard look 40 years later in the era of gene-environment interactions.American journal of physiology. Renal physiology · 2024Review
- An Update on Viral Infection-Associated Collapsing Glomerulopathy.Advances in kidney disease and health · 2024Review
- APOL1-G2 accelerates nephrocyte cell death by inhibiting the autophagy pathway.Disease models & mechanisms · 2023Article
- Recent Advances in Proteinuric Kidney Disease/Nephrotic Syndrome: Lessons from Knockout/Transgenic Mouse Models.Biomedicines · 2023Review
- NEF-Induced HIV-Associated Nephropathy Through HCK/LYN Tyrosine Kinases.The American journal of pathology · 2023Article
- Parietal Epithelial Cell Behavior and Its Modulation by microRNA-193a.Biomolecules · 2023Review
- Variant APOL1 protein in plasma associates with larger particles in humans and mouse models of kidney injury.PloS one · 2022Article
- APOL1 risk variants and the development of HIV-associated nephropathy.The FEBS journal · 2021Review
- Article
- Circulating fibroblast growth factor-2 precipitates HIV nephropathy in mice.Disease models & mechanisms · 2021Article
- Apolipoprotein L1 and mechanisms of kidney disease susceptibility.Current opinion in nephrology and hypertension · 2021Review
- Podocyte density is reduced in kidney allografts with high-risk APOL1 genotypes at transplantation.Clinical transplantation · 2021Article
- Inhibition of apoptosis signal-regulating kinase 1 mitigates the pathogenesis of human immunodeficiency virus-associated nephropathy.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2021Article
- Lessons From APOL1 Animal Models.Frontiers in medicine · 2021Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
African polymorphisms in the gene for Apolipoprotein L1 (APOL1) confer a survival advantage against lethal trypanosomiasis but also an increased risk for several chronic kidney diseases (CKD) including HIV-associated nephropathy (HIVAN). APOL1 is expressed in renal cells, however, the pathogenic events that lead to renal cell damage and kidney disease are not fully understood. The podocyte function of APOL1-G0 versus APOL1-G2 in the setting of a known disease stressor was assessed using transgenic mouse models. Transgene expression, survival, renal pathology and function, and podocyte density were assessed in an intercross of a mouse model of HIVAN (Tg26) with two mouse models that express either APOL1-G0 or APOL1-G2 in podocytes. Mice that expressed HIV genes developed heavy proteinuria and glomerulosclerosis, and had significant losses in podocyte numbers and reductions in podocyte densities. Mice that co-expressed APOL1-G0 and HIV had preserved podocyte numbers and densities, with fewer morphologic manifestations typical of HIVAN pathology. Podocyte losses and pathology in mice co-expressing APOL1-G2 and HIV were not significantly different from mice expressing only HIV. Podocyte hypertrophy, a known compensatory event to stress, was increased in the mice co-expressing HIV and APOL1-G0, but absent in the mice co-expressing HIV and APOL1-G2. Mortality and renal function tests were not significantly different between groups. APOL1-G0 expressed in podocytes may have a protective function against podocyte loss or injury when exposed to an environmental stressor. This was absent with APOL1-G2 expression, suggesting APOL1-G2 may have lost this protective function.
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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.