Evidence map›Paper›PMID 41266619›Full record

ReviewEye (London, England)2026

Pathobiology of the developing eye lens: regulation of intracellular MAPK-signalling pathways to prevent lens dysplasia.

Frank J Lovicu

Abstract readReview
In one paragraph

Review in Eye (London, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

1 author.

Frank J LovicuProfessor of Ocular Cell and Developmental Biology, Save Sight Institute and School of Medical Sciences, The University of Sydney, Sydney, NSW, Australia. frank.lovicu@sydney.edu.au.ORCID 0000-0001-5492-9200

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathobiology of the developing eye lens can result from a wide range of developmental defects, triggered by a range of mechanisms emanating from genetic mutations, intrauterine infections, metabolic and anatomical disorders, or extrinsic environmental factors. In this brief review we touch on the significance of the growth factor rich milieu of the ocular media that orchestrates the tight regulation of lens cellular processes essential for its distinct architecture. We take a closer look at select receptor tyrosine kinase pathways in lens, and some of the endogenous antagonists that negatively modulate them in return. The importance of preserving sight is showcased here through the plasticity of the lens responding to its environment, even when genetically modified to compromise its normal molecular machinery. Interestingly, opposing experimental approaches disrupting specific kinase phosphorylation in lens, that result in either heightened or reduced signalling activity, lead to similar pathological outcomes in the lens and eye, highlighting their important reciprocal relationship. We explore how the lens manages with different stresses to restore its homeostasis and balance as a means of maintaining its essential structure and associated functionality.

Indexed as

Lens, CrystallineLens DiseasesMAP Kinase Signaling SystemAnimalsHumansSignal Transduction

Identifiers

PMID41266619
PMCPMC12764570

What Socratic holds

Textmetadata
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.