Evidence map›Paper›PMID 25593510›Full record

Trial reportMolecular vision2015

Attenuation of lysyl oxidase and collagen gene expression in keratoconus patient corneal epithelium corresponds to disease severity.

Rohit Shetty, Arunapriya Sathyanarayanamoorthy, Reshma Airody Ramachandra, Vishal Arora, Anuprita Ghosh, Purnima Raman Srivatsa, Natasha Pahuja, Rudy M M A Nuijts, Abhijit Sinha-Roy, Rajiv R Mohan and 1 more

Abstract readClinical Trial
In one paragraph

Trial report in Molecular vision, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 3 pooled it
7.8field-weighted citation impact, top 2% 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

66 citing papers in PubMed, 3 syntheses or guidelines pooled it, 101 citations in OpenAlex.

  1. Pooled it
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  4. Update on the Physiopathology of Keratoconus.Medical sciences (Basel, Switzerland) · 2026
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6 more citing papers are in PubMed but not listed here.

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

11 authors at 1 institution in 1 country.

Rohit ShettyCornea Department, Narayana Nethralaya, Bangalore, India.
Arunapriya SathyanarayanamoorthyGROW Research Laboratory, Narayana Nethralaya Foundation, Bangalore, India.
Reshma Airody RamachandraGROW Research Laboratory, Narayana Nethralaya Foundation, Bangalore, India.
Vishal AroraCornea Department, Narayana Nethralaya, Bangalore, India.
Anuprita GhoshGROW Research Laboratory, Narayana Nethralaya Foundation, Bangalore, India.
Purnima Raman SrivatsaCornea Department, Narayana Nethralaya, Bangalore, India.
Natasha PahujaCornea Department, Narayana Nethralaya, Bangalore, India.
Rudy M M A NuijtsCornea Clinic, Department of Ophthalmology, Maastricht University Medical Center, Netherlands.
Abhijit Sinha-RoyGROW Research Laboratory, Narayana Nethralaya Foundation, Bangalore, India.
Rajiv R MohanMason Eye Institute, School of Medicine, University of Missouri-Columbia, Columbia, NY.
Arkasubhra GhoshGROW Research Laboratory, Narayana Nethralaya Foundation, Bangalore, India ; Singapore Eye Research Institute, Singapore.
Narayana Nethralaya · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeKeratoconus (KC) is characterized by progressive vision loss due to corneal thinning and structural abnormalities. It is hypothesized that KC is caused by deregulated collagen levels and collagen fibril-maturating enzyme lysyl oxidase (LOX). Further, it is currently not understood whether the gene expression deregulated by the corneal epithelium influences KC pathogenesis. We studied (i) the expressions of the LOX, collagen I (COL IA1), collagen IV (COL IVA1), MMP9, and IL6 genes in KC corneal epithelia, (ii) validated their expression levels in patient tissues, and (iii) correlated expression levels with KC disease severity. The primary goal of this study was to evaluate the importance of these genes in the progression of KC.

methodsWe analyzed the gene expression levels of the key proteins LOX, collagens (COL IA1 and COL IVA1), MMP9, and IL6 in debrided corneal epithelia from a large cohort of KC patients (90 eyes) and compared them to control patients (52 eyes) without KC. We measured the total LOX activity in the tears of KC patients compared to controls. We also correlated the protein expression levels of LOX and collagens by immunohistochemistry (IHC) in primary tissues from KC patients (27 eyes) undergoing keratoplasty compared to healthy donor corneas (15 eyes).

resultsWe observed a significant reduction in LOX transcript levels in KC corneal epithelia, and LOX activity in KC tears correlated with disease severity. Collagen transcripts were also reduced in KC while MMP9 transcript levels were upregulated and correlated with disease severity. IL6 was moderately increased in KC patients. IHC demonstrated a reduction in the protein expression levels of LOX in the epithelium and collagen IV in the basement membrane of KC patients compared to healthy donor corneas.

conclusionsThe data demonstrates that the structural deformity of the KC cornea may be dependent on reduced expressions of collagens and LOX, as well as on MMP9 elevated by the corneal epithelium.

Indexed as

AdultCase-Control StudiesCollagen Type ICollagen Type IVEpithelium, CornealFemaleGene Expression RegulationHumansInterleukin-6KeratoconusMaleMatrix Metalloproteinase 9Protein-Lysine 6-OxidaseRNA, MessengerSeverity of Illness IndexTearsCollagen Type ICollagen Type IVIL6 protein, humanInterleukin-6Matrix Metalloproteinase 9MMP9 protein, humanProtein-Lysine 6-OxidaseRNA, Messenger

Identifiers

PMID25593510
PMCPMC4301596
OpenAlexW7389565

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

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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.