Evidence map›Paper›PMID 29110761›Full record

ReviewSeminars in nephrology2017

The Cell Biology of APOL1.

John F O'Toole, Leslie A Bruggeman, Sethu Madhavan, John R Sedor

Abstract readReview
In one paragraph

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 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

28 citing papers in PubMed.

  1. Trial
  2. Molecular Mechanisms of APOL1-Associated Kidney Disease.International journal of molecular sciences · 2026
    Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Novel Therapies inKidney international reports · 2023
    Review
  10. Association betweeneLife · 2023
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Frontiers in genetics · 2022
    Article
  16. Article
  17. Article
  18. Kidney disease and APOL1.Human molecular genetics · 2021
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

John F O'TooleDepartment of Medicine, Case Western Reserve University, Cleveland, OH; Division of Nephrology, MetroHealth System, Cleveland, OH. Electronic address: otoolej@ccf.org.
Leslie A BruggemanDepartment of Medicine, Case Western Reserve University, Cleveland, OH; Division of Nephrology, MetroHealth System, Cleveland, OH.
Sethu MadhavanDepartment of Medicine, Case Western Reserve University, Cleveland, OH; Division of Nephrology, MetroHealth System, Cleveland, OH.
John R SedorDepartment of Medicine, Case Western Reserve University, Cleveland, OH; Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, OH; Division of Nephrology, MetroHealth System, Cleveland, OH.

Funding

Clinical and Translational Science Collaborative of ClevelandUL1TR000439 · NCATS · CASE WESTERN RESERVE UNIVERSITY · PI KONSTAN, MICHAEL W. · 2012 to 2016
$50.0M
Zosuquidar trihydrochloride for acute myeloid leukemia &refractory anemiaM01RR000080 · NCRR · UNIVERSITY HOSPITALS OF CLEVELAND · PI DAVIS, PAMELA B · 1985 to 2007
$22.2M
CWRU NEPHROLOGY TRAINING PROGRAMT32DK007470 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI SEDOR, JOHN R. · 1986 to 2019
$2.9M
Mechanisms of APOL1-mediated kidney diseaseR01DK108329 · NIDDK · CLEVELAND CLINIC LERNER COM-CWRU · PI BRUGGEMAN, LESLIE A, O'TOOLE, JOHN F. · 2015 to 2019
$2.0M
Kidney disease mechanisms associated with human genetic variationR01DK097836 · NIDDK · CLEVELAND CLINIC LERNER COM-CWRU · PI BRUGGEMAN, LESLIE A, O'TOOLE, JOHN F. · 2014 to 2017
$2.0M
Kidney disease mechanisms associated with human genetic variationR56DK097836 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI BRUGGEMAN, LESLIE A, O'TOOLE, JOHN F. · 2012 to 2012
$198k
NCATS NIH HHS UL1 TR000439NCRR NIH HHS M01 RR000080NIDDK NIH HHS R01 DK097836NIDDK NIH HHS R01 DK108329NIDDK NIH HHS R56 DK097836NIDDK NIH HHS T32 DK007470
6 · The paper itself

Abstract

The association of variants in the APOL1 gene, which encodes apolipoprotein L1 (APOL1), with progressive nondiabetic kidney diseases in African Americans has prompted intense investigation into the function(s) of APOL1. APOL1 is an innate immune effector that protects human beings from infection by some trypanosomal parasites. We review the data characterizing APOL1 trypanolytic function, which has been a basis for studies of APOL1 function in mammalian cells. Subsequently, we discuss the studies that use animal models, mammalian cell culture models, and kidney biopsy tissue to discover the mechanisms of variant APOL1-associated kidney diseases.

Indexed as

AnimalsAntigens, NeoplasmApolipoprotein L1HaptoglobinsHumansImmunity, InnatePodocytesRenal Insufficiency, ChronicSignal TransductionTrypanosomiasis, AfricanAntigens, NeoplasmAPOL1 protein, humanApolipoprotein L1HaptoglobinsHPR protein, humanAfrican Americancytotoxicityion channelKidney diseasetrypanosome

Identifiers

PMID29110761
PMCPMC5678957

What OpenQuestion holds

Textmetadata
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Read underepoch 390

Registered trials

None linked

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.