Evidence map›Paper›PMID 25580276›Full record

ArticleJournal of clinical medicine2014

Inflammation and Cell Death in Age-Related Macular Degeneration: An Immunopathological and Ultrastructural Model.

Christopher P Ardeljan, Daniel Ardeljan, Mones Abu-Asab, Chi-Chao Chan

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
4.0field-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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Frontiers in veterinary science · 2026
    Article
  4. Observational
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Damage-Associated Molecular Patterns (DAMPs) in Retinal Disorders.International journal of molecular sciences · 2022
    Review
  12. An Ultrastructural Perspective on Cell Death.Jordan medical journal · 2022
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  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 3 institutions in 1 country.

Christopher P ArdeljanHistology Core, Laboratory of Immunology, National Eye Institute/National Institutes of Health, Bethesda, Maryland 20892-1857, MD, USA.
Daniel ArdeljanHuman Genetics Program, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, MD, USA.
Mones Abu-AsabHistology Core, Laboratory of Immunology, National Eye Institute/National Institutes of Health, Bethesda, Maryland 20892-1857, MD, USA.
Chi-Chao ChanHistology Core, Laboratory of Immunology, National Eye Institute/National Institutes of Health, Bethesda, Maryland 20892-1857, MD, USA ; Immunopathology Section, Laboratory of Immunology, National Eye Institute/National Institutes of Health, Bethesda, Maryland 20892-1857, MD, USA.
National Eye Institute · USJohns Hopkins Medicine · USNational Institutes of Health · US

Funding

Histopathology CoreZICEY000461 · NEI · NATIONAL EYE INSTITUTE · PI SCHNEEWEIS, DAVID · 2009 to 2022
$7.7M
Molecular And Immunopathology Of Experimental And Clinical Ocular DiseasesZIAEY000222 · NEI · NATIONAL EYE INSTITUTE · PI CHAN, CHI-CHAO · 2009 to 2015
$7.2M
Age-Related Macular Degeneration: Genetic Variations and Animal ModelZIAEY000418 · NEI · NATIONAL EYE INSTITUTE · PI CHAN, CHI-CHAO · 2009 to 2015
$6.0M
Intramural NIH HHS ZIA EY000222Intramural NIH HHS ZIA EY000418Intramural NIH HHS ZIC EY000461
6 · The paper itself

Abstract

The etiology of Age-related Macular Degeneration (AMD) remains elusive despite the characterization of many factors contributing to the disease in its late-stage phenotypes. AMD features an immune system in flux, as shown by changes in macrophage polarization with age, expression of cytokines and complement, microglial accumulation with age, etc. These point to an allostatic overload, possibly due to a breakdown in self vs. non-self when endogenous compounds and structures acquire the appearance of non-self over time. The result is inflammation and inflammation-mediated cell death. While it is clear that these processes ultimately result in degeneration of retinal pigment epithelium and photoreceptor, the prevalent type of cell death contributing to the various phenotypes is unknown. Both molecular studies as well as ultrastructural pathology suggest pyroptosis, and perhaps necroptosis, are the predominant mechanisms of cell death at play, with only minimal evidence for apoptosis. Herein, we attempt to reconcile those factors identified by experimental AMD models and integrate these data with pathology observed under the electron microscope-particularly observations of mitochondrial dysfunction, DNA leakage, autophagy, and cell death.

Indexed as

age-related macular degeneration (AMD)apoptosisautophagycytokineinflammasomemacrophagemicroglianecroptosispyroptosis

Identifiers

PMID25580276
PMCPMC4287551
OpenAlexW2123131667

What OpenQuestion 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 OpenQuestion graph.