ReviewTrends in molecular medicine2018
APOL1: The Balance Imposed by Infection, Selection, and Kidney Disease.
Review in Trends in molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Phenome-wide association analysis suggests the APOL1 linked disease spectrum primarily drives kidney-specific pathways.Kidney international · 2020Pooled it
- Update on APOL1 and chronic kidney diseases in children.Pediatric nephrology (Berlin, Germany) · 2026Review
- Coding, modifier, and regulatory effects shape circulating APOL1 levels.Human molecular genetics · 2026Article
- APOL1 kidney disease: a critical narrative review of molecular mechanisms, clinical heterogeneity, and the emerging therapeutic landscape.International urology and nephrology · 2026Review
- The impact of cardiovascular risk factors in non-classical Fabry disease.Orphanet journal of rare diseases · 2026Article
- Nephrotic syndrome genomic discovery in the Mass General Brigham Biobank identifies monoallelic MEFV variants as a risk factor for focal segmental glomerulosclerosis.Kidney international · 2026Article
- Molecular mechanisms in podocytopathies: finding suitable targets for a new era of glomerular gene therapy.Clinical kidney journal · 2026Review
- GDIv2: improving variant selection from human exomes.Bioinformatics advances · 2026Article
- Review
- Interferon-γ induces combined pyroptotic angiopathy and APOL1 expression in human kidney disease.Cell reports · 2024Article
- A human-specific insertion promotes cell proliferation and migration by enhancing TBC1D8B expression.Science China. Life sciences · 2024Article
- IFI16 Is Indispensable for Promoting HIF-1α-Mediated APOL1 Expression in Human Podocytes under Hypoxic Conditions.International journal of molecular sciences · 2024Article
- Phenome-wide analysis reveals epistatic associations between APOL1 variants and chronic kidney disease and multiple other disorders.EBioMedicine · 2024Article
- Apolipoproteins L1 and L3 control mitochondrial membrane dynamics.Cell reports · 2023Article
- APOL1-G2 accelerates nephrocyte cell death by inhibiting the autophagy pathway.Disease models & mechanisms · 2023Article
- Genetic Susceptibility to Chronic Kidney Disease: Links, Risks and Management.International journal of nephrology and renovascular disease · 2023Review
- Antisense oligonucleotides ameliorate kidney dysfunction in podocyte-specific APOL1 risk variant mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2022Article
- Inhibition of endoplasmic reticulum stress signaling rescues cytotoxicity of human apolipoprotein-L1 risk variants in Drosophila.Kidney international · 2022Article
- The evolving story of apolipoprotein L1 nephropathy: the end of the beginning.Nature reviews. Nephrology · 2022Review
- APOL1 Risk Variants, Acute Kidney Injury, and Death in Participants With African Ancestry Hospitalized With COVID-19 From the Million Veteran Program.JAMA internal medicine · 2022Article
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 1 institution in 2 countries.
Funding
Abstract
Chronic kidney disease (CKD) affects millions of people and constitutes a major health and financial burden worldwide. People of African descent are at an increased risk of developing kidney disease, which is mostly explained by two variants in the Apolipoprotein L1 (APOL1) gene that are found only in people of west African origin. It is hypothesized that these variants were genetically selected due to the protection they afford against African sleeping sickness, caused by the parasite Trypanosoma brucei. Targeting mutant APOL1 could have substantial therapeutic potential for treating kidney disease. In this review, we will describe the intriguing interplay between microbiology, genetics, and kidney disease as revealed in APOL1-associated kidney disease, discuss APOL1-induced cytotoxicity and its therapeutic implications.
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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.