Evidence map›Paper›PMID 28265848›Full record

ReviewCurrent rheumatology reports2017

ApoL1 and the Immune Response of Patients with Systemic Lupus Erythematosus.

Ashira D Blazer, Robert M Clancy

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current rheumatology reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

9 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Frontiers in genetics · 2022
    Article
  6. Article
  7. Lessons From APOL1 Animal Models.Frontiers in medicine · 2021
    Review
  8. Article
  9. 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

2 authors at 1 institution in 1 country.

Ashira D BlazerDivision of Rheumatology, Department of Medicine, New York University School of Medicine, 550 First Avenue, MSB 611, New York, NY, 10016, USA. ashira.blazer@nyumc.org.
Robert M ClancyDivision of Rheumatology, Department of Medicine, New York University School of Medicine, 550 First Avenue, MSB 611, New York, NY, 10016, USA.
New York University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewSystemic lupus erythematosus (SLE) confers up to a 50-fold increased risk of cardiovascular disease (CVD), and African Americans with SLE experience accelerated damage accrual and doubled cardiovascular risk when compared to their European American counterparts. RECENT

findingsGenome-wide association studies have identified a substantial signal at 22q13, now assigned to variation at apolipoprotein L1 (APOL1), which has associated with progressive nondiabetic nephropathy, cardiovascular disease, and many immune-associated renal diseases, including lupus nephritis. We contend that alterations in crucial APOL1 intracellular pathways may underpin associated disease states based on structure-functional differences between variant and ancestral forms. While ancestral APOL1 may be a key driver of autophagy, nonconserved primary structure changes result in a toxic gain of function with attenuation of autophagy and an unsupervised pore-forming feature. Thus, the divergent intracellular biological pathways of ancestral and variant APOL1 may explain a worsened prognosis as demonstrated in SLE.

Indexed as

Apolipoprotein L1ApolipoproteinsAutophagyCardiovascular DiseasesGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansLipoproteins, HDLLupus Erythematosus, SystemicLupus NephritisAPOL1 protein, humanApolipoprotein L1ApolipoproteinsLipoproteins, HDLAutoimmunityAutophagyFunctional genetics

Identifiers

PMID28265848
OpenAlexW2593537865

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.