Evidence map›Paper›PMID 26318017›Full record

ReviewBiochimica et biophysica acta2016

The etiology of human age-related cataract. Proteins don't last forever.

Roger J W Truscott, Michael G Friedrich

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Biochimica et biophysica acta, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
5.7field-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

55 citing papers in PubMed, 113 citations in OpenAlex.

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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 at 1 institution in 1 country.

Roger J W TruscottIllawarra Health and Medical Research Institute, University of Wollongong, Wollongong, NSW, 2522, Australia. Electronic address: rjwt@uow.edu.au.
Michael G FriedrichIllawarra Health and Medical Research Institute, University of Wollongong, Wollongong, NSW, 2522, Australia.
University of Wollongong · AU

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 EY024258NEI NIH HHS R01EY024258
6 · The paper itself

Abstract

backgroundIt is probable that the great majority of human cataract results from the spontaneous decomposition of long-lived macromolecules in the human lens. Breakdown/reaction of long-lived proteins is of primary importance and recent proteomic analysis has enabled the identification of the particular crystallins, and their exact sites of amino acid modification. SCOPE OF REVIEW: Analysis of proteins from cataractous lenses revealed that there are sites on some structural proteins that show a consistently greater degree of deterioration than age-matched normal lenses. MAJOR

conclusionsThe most abundant posttranslational modification of aged lens proteins is racemization. Deamidation, truncation and crosslinking, each arising from the spontaneous breakdown of susceptible amino acids within proteins, are also present. Fundamental to an understanding of nuclear cataract etiology, it is proposed that once a certain degree of modification at key sites occurs, that protein-protein interactions are disrupted and lens opacification ensues. GENERAL SIGNIFICANCE: Since long-lived proteins are now recognized to be present in many other sites of the body, such as the brain, the information gleaned from detailed analyses of degraded proteins from aged lenses will apply more widely to other age-related human diseases. This article is part of a Special Issue entitled Crystallin Biochemistry in Health and Disease.

Indexed as

AgingAnimalsCataractCrystallinsHumansLens, CrystallineModels, BiologicalModels, ChemicalProtein DenaturationProtein FoldingCrystallinsCrystallinsHuman agingLensLifespanProtein degradation

Identifiers

PMID26318017
PMCPMC5489112
OpenAlexW1229018818

What OpenQuestion holds

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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.