Evidence map›Paper›PMID 42653325›Full record

ArticleInternational journal of molecular sciences2026

Insulin-like Growth Factor Signaling Promotes Corneal Myofibroblast Survival and Sustains Corneal Fibrosis.

Yunjeong Hwang, Kyung-No Son, Manoj Chaudhary, Eunbee Lee, Minhyung Kim, Sungyong You, Terry J Smith, Vinay Kumar Aakalu, Kyu-Yeon Han

Abstract read
In one paragraph

Article in International journal of molecular sciences, 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

9 authors.

Yunjeong HwangDepartment of Ophthalmology and Visual Sciences, Illinois Eye and Ear Infirmary, College of Medicine, University of Illinois Chicago, Chicago, IL 60612, USA.
Kyung-No SonDepartment of Ophthalmology and Visual Sciences, Eye Institute, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Manoj ChaudharyDepartment of Ophthalmology and Visual Sciences, Eye Institute, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Eunbee LeeDepartment of Ophthalmology and Visual Sciences, Illinois Eye and Ear Infirmary, College of Medicine, University of Illinois Chicago, Chicago, IL 60612, USA.
Minhyung KimDepartments of Urology and Computational Biomedicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Sungyong YouDepartments of Urology and Computational Biomedicine, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Terry J SmithDepartment of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48105, USA.ORCID 0000-0002-6279-9685
Vinay Kumar AakaluDepartment of Ophthalmology and Visual Sciences, Eye Institute, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
Kyu-Yeon HanDepartment of Ophthalmology and Visual Sciences, Illinois Eye and Ear Infirmary, College of Medicine, University of Illinois Chicago, Chicago, IL 60612, USA.ORCID 0000-0002-2561-8187

Funding

Translational Core for Therapeutic and Diagnostic DevelopmentP30EY001792 · NEI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MCANANY, JAMES JASON · 1985 to 2025
$14.8M
Identification of a new role of membrane‐type 1 matrix metalloproteinases in corneal neovascularizationR01EY033758 · NEI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI Kyuyeon Han · 2023 to 2026
$1.6M
NEI NIH HHS P30 EY001792NEI NIH HHS R01 EY033758NIH HHS 4R01EY033758-58
6 · The paper itself

Abstract

Corneal fibrosis is a major cause of visual impairment worldwide and is characterized by persistent stromal scarring that disrupts corneal transparency. Although transforming growth factor-β (TGF-β)-mediated myofibroblast differentiation is well established, the mechanisms that sustain myofibroblast survival and persistence remain poorly understood. In this study, we investigated the role of the insulin-like growth factor (IGF) signaling axis in corneal myofibroblast survival and evaluated the therapeutic potential of linsitinib, a dual IGF-1 receptor (IGF-1R)/insulin receptor (INSR) inhibitor. Primary corneal myofibroblasts were exposed to pro-apoptotic conditions and treated with IGF ligands in the presence or absence of linsitinib. The effects of IGF pathway inhibition were further examined in a mouse model of corneal fibrosis. IGF-1 and IGF-2 promoted myofibroblast survival under pro-apoptotic conditions, whereas pharmacologic inhibition of IGF-1R/INSR signaling with linsitinib blocked these pro-survival effects. In vivo, linsitinib treatment reduced myofibroblast persistence and attenuated corneal fibrosis. These findings identify the IGF axis as a critical regulator of corneal myofibroblast survival and suggest that persistent fibrosis is maintained, in part, by IGF-dependent resistance to apoptosis. Targeting survival pathways rather than myofibroblast differentiation may represent a novel therapeutic strategy for the treatment of corneal fibrosis.

Indexed as

CorneaCorneal DiseasesInsulin-Like Growth Factor IInsulin-Like PeptidesMyofibroblastsSignal TransductionAnimalsApoptosisCell DifferentiationCells, CulturedCell SurvivalFibrosisImidazolesInsulin-Like Growth Factor IIMiceMice, Inbred C57BL3-(8-amino-1-(2-phenylquinolin-7-yl)imidazo(1,5-a)pyrazin-3-yl)-1-methylcyclobutanolImidazolesInsulin-Like Growth Factor IInsulin-Like Growth Factor IIInsulin-Like PeptidesPyrazinesReceptor, IGF Type 1corneal fibrosisInsulin-like growth factorlinsitinib

Identifiers

PMID42653325
PMCPMC13513157

What OpenQuestion 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 OpenQuestion graph.