Evidence mapPaperPMID 25280384Full record

SynthesisBMC medical genetics2014

Meta-analysis of diabetic nephropathy associated genetic variants in inflammation and angiogenesis involved in different biochemical pathways.

Nyla Nazir, Khalid Siddiqui, Sara Al-Qasim, Dhekra Al-Naqeb

Open access · goldAbstract readMeta-Analysis
In one paragraph

Synthesis in BMC medical genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 2 pooled it
3.5field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 2 syntheses or guidelines pooled it, 56 citations in OpenAlex.

  1. The Role ofGenes · 2025
    Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Review
  7. The Role of Platelets in Diabetic Kidney Disease.International journal of molecular sciences · 2022
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. The Susceptibility Genes in Diabetic Nephropathy.Kidney diseases (Basel, Switzerland) · 2018
    Review
  18. Article
  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 at 1 institution in 1 country.

Nyla NazirStrategic Center for Diabetes Research, King Saud University, P.O. Box 18397, Riyadh, 11415, K.S.A, Saudi Arabia. npeerzada@ksu.edu.sa.
Khalid SiddiquiStrategic Center for Diabetes Research, King Saud University, P.O. Box 18397, Riyadh, 11415, K.S.A, Saudi Arabia. ksiddiqui@ksu.edu.sa.
Sara Al-QasimStrategic Center for Diabetes Research, King Saud University, P.O. Box 18397, Riyadh, 11415, K.S.A, Saudi Arabia. sqassim@dsrcenter.org.
Dhekra Al-NaqebStrategic Center for Diabetes Research, King Saud University, P.O. Box 18397, Riyadh, 11415, K.S.A, Saudi Arabia. dalnaqeb@dsrcenter.org.
King Saud University · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiabetes mellitus is the most common chronic endocrine disorder, affecting an estimated population of 382 million people worldwide. It is associated with microvascular and macrovascular complications, including diabetic nephropathy (DN); primary cause of end-stage renal disease. Different inflammatory and angiogenic molecules in various pathways are important modulators in the pathogenesis and progression of diabetic nephropathy. Differential disease risk in DN may be partly attributable to genetic susceptibility. In this meta-analysis, we aimed to determine which of the previously investigated genetic variants in these pathways are significantly associated with the development of DN and to examine the functional role of these genes.

methodsA systematic search was conducted to collect and analyze all studies published till June 2013; that investigated the association between genetic variants involved in inflammatory cytokines and angiogenesis and diabetic nephropathy. Genetic variants associated with DN were selected and analyzed by using Comprehensive Meta Analysis software. Pathway analysis of the genes with variants showing significant positive association with DN was performed using Genomatix Genome Analyzer (Genomatix, Munich, Germany).

resultsAfter the inclusion and exclusion criteria for this analysis, 34 studies were included in this meta-analysis. 11 genetic variants showed significant positive association with DN in a random-effects meta-analysis. These included genetic variants within or near VEGFA, CCR5, CCL2, IL-1, MMP9, EPO, IL-8, ADIPOQ and IL-10. rs1800871 (T) genetic variant in IL-10 showed protective effect for DN. Most of these eleven genetic variants were involved in GPCR signaling and receptor binding pathways whereas four were involved in chronic kidney failure. rs833061 [OR 2.08 (95% CI 1.63-2.66)] in the VEGFA gene and rs3917887 [OR 2.04 (95% CI 1.64-2.54)] in the CCL2 gene showed the most significant association with the risk of diabetic nephropathy.

conclusionsOur results indicate that 11 genetic variants within or near VEGFA, CCR5, CCL2, IL-1, MMP9, EPO, IL-8, ADIPOQ and IL-10 showed significant positive association with diabetic nephropathy. Gene Ontology or pathway analysis showed that these genes may contribute to the pathophysiology of DN. The functional relevance of the variants and their pathways can lead to increased biological insights and development of new therapeutic targets.

Indexed as

Chemokine CCL2Databases, BibliographicDiabetic NephropathiesGene Regulatory NetworksGenetic Association StudiesGenetic Predisposition to DiseaseGenetic VariationHumansInflammationVascular Endothelial Growth Factor ACCL2 protein, humanChemokine CCL2Vascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID25280384
PMCPMC4411872
OpenAlexW2101323147

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.