ReviewSeminars in nephrology2017
APOL1 Nephrotoxicity: What Does Ion Transport Have to Do With It?
Review in Seminars in nephrology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed, 21 citations in OpenAlex.
- Alterations in DNA Methylation, Proteomic, and Metabolomic Profiles in African Ancestry Populations with APOL1 Risk Alleles.Journal of the American Society of Nephrology : JASN · 2025Article
- Podocyte-targeted therapies - progress and future directions.Nature reviews. Nephrology · 2024Review
- Collapsing Glomerulopathy.Advances in kidney disease and health · 2024Review
- Multi-ancestry GWAS analysis identifies two novel loci associated with diabetic eye disease and highlights APOL1 as a high risk locus in patients with diabetic macular edema.PLoS genetics · 2023Article
- Apolipoprotein L1 (APOL1) cation current in HEK-293 cells and in human podocytes.Pflugers Archiv : European journal of physiology · 2023Article
- Novel Treatment Paradigms: Focal Segmental Glomerulosclerosis.Kidney international reports · 2023Review
- The evolving story of apolipoprotein L1 nephropathy: the end of the beginning.Nature reviews. Nephrology · 2022Review
- APOL1 G3 Variant Is Associated with Cardiovascular Mortality and Sudden Cardiac Death in Patients Receiving Maintenance Hemodialysis of European Ancestry.Cardiorenal medicine · 2022Article
- APOL1 risk variants in kidney transplantation: a modulation of immune cell function.The Journal of clinical investigation · 2021Article
- APOL1 at 10 years: progress and next steps.Kidney international · 2021Article
- Domain-Specific Antibodies Reveal Differences in the Membrane Topologies of Apolipoprotein L1 in Serum and Podocytes.Journal of the American Society of Nephrology : JASN · 2020Article
- Racial and health insurance disparities in pediatric acute kidney injury in the USA.Pediatric nephrology (Berlin, Germany) · 2020Article
- Alterations in plasma membrane ion channel structures stimulate NLRP3 inflammasome activation in APOL1 risk milieu.The FEBS journal · 2020Article
- Article
- APOL1: The Balance Imposed by Infection, Selection, and Kidney Disease.Trends in molecular medicine · 2018Review
- Apolipoprotein L1 nephropathies: 2017 in review.Current opinion in nephrology and hypertension · 2018Review
- Genetic risk of APOL1 and kidney disease in children and young adults of African ancestry.Current opinion in pediatrics · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Apolipoprotein L1 (APOL1) protein is the human serum factor that protect human beings against Trypanosoma brucei brucei, the cause of trypanosomiasis. Subspecies of T b brucei that cause human sleeping sickness-T b gambiense and T b rhodesiense evolved molecular mechanisms that enabled them to evade killing by APOL1. Sequence changes (termed G1 and G2) in the APOL1 gene that restored its ability to kill T b rhodesiense also increase the risk of developing glomerular diseases and accelerate progression to end-stage kidney disease. To lyse trypanosome parasites, APOL1 forms pores in the trypanosome endolysosomal and mitochondrial membranes, resulting in rapid membrane depolarization. However, the molecular mechanism underlying APOL1 nephropathy is unknown. Recent experimental evidence has shown that aberrant efflux of intracellular potassium is an early event in APOL1-induced death of human embryonic kidney cells. Here, we discuss the possibility that abnormal efflux of cellular potassium or other cations may be relevant to the pathogenesis of APOL1 nephropathy.
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What OpenQuestion holds
Registered trials
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.