Evidence map›Paper›PMID 26994570›Full record

ArticleKidney international2016

Targeting the fatty acid transport protein CD36, a class B scavenger receptor, in the treatment of renal disease.

Hideki Yokoi, Motoko Yanagita

Open access · bronzeAbstract readComment
PubMed Publisher
In one paragraph

Article in Kidney international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 10% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
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  12. Observational
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  20. Kidney Damage Caused by Obesity and Its Feasible Treatment Drugs.International journal of molecular sciences · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Hideki YokoiDepartment of Nephrology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Motoko YanagitaDepartment of Nephrology, Kyoto University Graduate School of Medicine, Kyoto, Japan. Electronic address: motoy@kuhp.kyoto-u.ac.jp.
Kyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Augmentation of the CD36 pathway, which involves the uptake of several endogenous ligands including free fatty acids and oxidized low-density lipoprotein, contributes to the damage of proximal tubules and podocytes, whereas ablation of CD36 attenuates renal injury. Souza et al. demonstrate that 5A peptide can inhibit CD36 signaling, attenuate chronic kidney disease progression, and ameliorate inflammation and tubulointerstitial fibrosis by reducing the expression of inflammatory cytokines and chemokines, suggesting the therapeutic potential of 5A peptide against CD36-mediated renal injury.

Indexed as

CD36 AntigensFatty Acid Transport ProteinsHumansKidney DiseasesLipoproteins, LDLPodocytesReceptors, ScavengerCD36 AntigensFatty Acid Transport ProteinsLipoproteins, LDLReceptors, Scavenger

Identifiers

PMID26994570
OpenAlexW2301299644

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.