Evidence map›Paper›PMID 29301530›Full record

SynthesisLipids in health and disease2018

Understanding AMD by analogy: systematic review of lipid-related common pathogenic mechanisms in AMD, AD, AS and GN.

Qinyuan Xu, Sijia Cao, Sanjeeva Rajapakse, Joanne A Matsubara

Open access · goldAbstract readSystematic Review
In one paragraph

Synthesis in Lipids in health and disease, 2018. 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
5.8field-weighted citation impact, top 3% 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, 52 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. The human factor H protein family - an update.Frontiers in immunology · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. NURR1 expression regulates retinal pigment epithelial-mesenchymal transition and age-related macular degeneration phenotypes.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  13. Review
  14. Review
  15. Article
  16. Targeting of miR-33 ameliorates phenotypes linked to age-related macular degeneration.Molecular therapy : the journal of the American Society of Gene Therapy · 2021
    Article
  17. Review
  18. 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 at 1 institution in 1 country.

Qinyuan XuDepartment of Ophthalmology and Visual Sciences, Faculty of Medicine, University of British Columbia, Vancouver, BC, V5Z 3N9, Canada.
Sijia CaoDepartment of Ophthalmology and Visual Sciences, Faculty of Medicine, University of British Columbia, Vancouver, BC, V5Z 3N9, Canada.
Sanjeeva RajapakseDepartment of Ophthalmology and Visual Sciences, Faculty of Medicine, University of British Columbia, Vancouver, BC, V5Z 3N9, Canada.
Joanne A MatsubaraDepartment of Ophthalmology and Visual Sciences, Faculty of Medicine, University of British Columbia, Vancouver, BC, V5Z 3N9, Canada. jms@mail.ubc.ca.
University of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rationaleAge-related macular degeneration (AMD) is one of the leading causes of blindness among the elderly. Due to its complex etiology, current treatments have been insufficient. Previous studies reveal three systems closely involved in AMD pathogenesis: lipid metabolism, oxidation and inflammation. These systems are also involved in Alzheimer's disease, atherosclerosis and glomerulonephritis. Understanding commonalities of these four diseases may provide insight into AMD etiology.

objectivesTo understand AMD pathogenesis by analogy and suggest ideas for future research, this study summarizes main commonalities in disease pathogenesis of AMD, Alzheimer's disease, atherosclerosis and glomerulonephritis.

methodsArticles were identified through PubMed, Ovid Medline and Google Scholar. We summarized the common findings and synthesized critical differences.

resultsOxidation, lipid deposition, complement activation, and macrophage recruitment are involved in all four diseases shown by genetic, molecular, animal and human studies. Shared genetic variations further strengthen their connection. Potential areas for future research are suggested throughout the review.

conclusionsThe four diseases share many steps of an overall framework of pathogenesis. Various oxidative sources cause oxidative stress. Oxidized lipids and related molecules accumulate and lead to complement activation, macrophage recruitment and pathology. Investigations that arise under this structure may aid us to better understand AMD pathology.

Indexed as

Alzheimer DiseaseAnimalsApolipoproteinsAtherosclerosisCholesterolComplement ActivationComplement System ProteinsGene ExpressionGenetic VariationGlomerulonephritisHumansInflammationLipid MetabolismMacrophagesMacular DegenerationOxidative StressApolipoproteinsCholesterolComplement System ProteinsApolipoproteinsCholesterolComplementDiseasesInflammationLipids/oxidationMacrophages

Identifiers

PMID29301530
PMCPMC5755337
OpenAlexW2782225202

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.