Evidence map›Paper›PMID 31791064›Full record

ReviewInvestigative ophthalmology & visual science2019

Molecular Processes Implicated in Human Age-Related Nuclear Cataract.

Roger J W Truscott, Michael G Friedrich

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Investigative ophthalmology & visual science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

46 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
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  7. Article
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  9. Article
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  11. Article
  12. Preventing Age-Related Nuclear Cataract Development - Is Cholesterol the Key?Investigative ophthalmology & visual science · 2026
    Review
  13. Review
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  15. Article
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  20. Metformin protects human lens epithelial cells from high glucose-induced senescence and autophagy inhibition by upregulating SIRT1.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2024
    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.

Roger J W TruscottIllawarra Health and Medical Research Institute, University of Wollongong, Australia.
Michael G FriedrichIllawarra Health and Medical Research Institute, University of Wollongong, Australia.

Funding

Mechanisms of Protein Aging in Normal and Cataractous LensesR01EY024258 · NEI · VANDERBILT UNIVERSITY · PI SCHEY, KEVIN L · 2014 to 2022
$2.6M
NEI NIH HHS R01 EY024258
6 · The paper itself

Abstract

Human age-related nuclear cataract is commonly characterized by four biochemical features that involve modifications to the structural proteins that constitute the bulk of the lens: coloration, oxidation, insolubility, and covalent cross-linking. Each of these is progressive and increases as the cataract worsens. Significant progress has been made in understanding the origin of the factors that underpin the loss of lens transparency. Of these four hallmarks of cataract, it is protein-protein cross-linking that has been the most intransigent, and it is only recently, with the advent of proteomic methodology, that mechanisms are being elucidated. A diverse range of cross-linking processes involving several amino acids have been uncovered. Although other hypotheses for the etiology of cataract have been advanced, it is likely that spontaneous decomposition of the structural proteins of the lens, which do not turn over, is responsible for the age-related changes to the properties of the lens and, ultimately, for cataract. Cataract may represent the first and best characterized of a number of human age-related diseases where spontaneous protein modification leads to ongoing deterioration and, ultimately, a loss of tissue function.

Indexed as

AgingCataractCrystallinsEye ProteinsHumansLens, CrystallineOxidation-ReductionProteomicsCrystallinsEye Proteins

Identifiers

PMID31791064
PMCPMC7043214

What OpenQuestion holds

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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.