Evidence map›Paper›PMID 29357411›Full record

ArticleAmerican journal of physiology. Renal physiology2018

ApoL1 renal risk variants induce aberrant THP-1 monocyte differentiation and increase eicosanoid production via enhanced expression of cyclooxygenase-2.

Hewang Lee, Hila Roshanravan, Ying Wang, Koji Okamoto, Junghwa Ryu, Shashi Shrivastav, Peng Qu, Jeffrey B Kopp

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.0field-weighted citation impact, top 27% of its field
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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. APOL1 and kidney cell function.American journal of physiology. Renal physiology · 2019
    Review
  9. Ten years in: APOL1 reaches beyond the kidney.Current opinion in nephrology and hypertension · 2019
    Review
  10. Article
  11. 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

8 authors at 4 institutions in 2 countries.

Hewang LeeInstitute of Heart and Vessel Diseases, Second Hospital, Dalian Medical University , Dalian , China.
Hila RoshanravanKidney Disease Section, Kidney Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health , Bethesda, Maryland.
Ying WangInstitute of Heart and Vessel Diseases, Second Hospital, Dalian Medical University , Dalian , China.
Koji OkamotoKidney Disease Section, Kidney Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health , Bethesda, Maryland.
Junghwa RyuKidney Disease Section, Kidney Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health , Bethesda, Maryland.
Shashi ShrivastavKidney Disease Section, Kidney Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health , Bethesda, Maryland.
Peng QuInstitute of Heart and Vessel Diseases, Second Hospital, Dalian Medical University , Dalian , China.
Jeffrey B KoppKidney Disease Section, Kidney Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health , Bethesda, Maryland.
National Institutes of Health · USSecond Affiliated Hospital of Dalian Medical University · CNDalian Medical University · CNNational Institute of Diabetes and Digestive and Kidney Diseases · US

Funding

Focal Segmental Glomerulosclerosis: Genetics & MechanismsZIADK043308 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI KOPP, JEFFREY BURNETT · 2009 to 2024
$15.7M
FOCAL SEGMENTAL GLOMERULOSCLEROSIS--PATHOGENESIS AND TREATMENTZ01DK043308 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI KOPP, JEFFREY BURNETT · 1997 to 2008
$1.0M
Intramural NIH HHS Z01 DK043308NIDDK NIH HHS Z01 DK043308
6 · The paper itself

Abstract

Apolipoprotein L1 ( ApoL1) genetic variants are strongly associated with kidney diseases. We investigated the role of ApoL1 variants in monocyte differentiation and eicosanoid production in macrophages, as activated tissue macrophages in kidney might contribute to kidney injury. In human monocyte THP-1 cells, transient overexpression of ApoL1 (G0, G1, G2) by transfection resulted in a 5- to 11-fold increase in CD14 and CD68 gene expression, similar to that seen with phorbol-12-myristate acetate treatment. All ApoL1 variants caused monocytes to differentiate into atypical M1 macrophages with marked increase in M1 markers CD80, TNF, IL1B, and IL6 and modest increase in the M2 marker CD163 compared with control cells. ApoL1-G1 transfection induced additional CD206 and TGFB1 expression, and ApoL1-G2 transfection induced additional CD204 and TGFB1 expression. Gene expression of prostaglandin E

Indexed as

Cell DifferentiationGenetic VariationMacrophage ActivationApolipoprotein L1BiomarkersCyclooxygenase 2DinoprostoneEicosanoidsHumansMacrophagesMonocytesPhenotypeSignal TransductionTHP-1 CellsThromboxane B2TransfectionAPOL1 protein, humanApolipoprotein L1BiomarkersCyclooxygenase 2DinoprostoneEicosanoidsPTGS2 protein, humanTGFB1 protein, humanThromboxane B2Transforming Growth Factor beta1apolipoprotein L1cyclooxygenase-2macrophage polarizationTGF-β1

Identifiers

PMID29357411
PMCPMC6087794
OpenAlexW2783447999

What OpenQuestion holds

Textmetadata
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.