Evidence map›Paper›PMID 40953793›Full record

ArticleDevelopmental biology2025

Hyperactive PDGFRβ signaling induces cataractogenesis via TGFβ and STAT5-IGF1.

Jesse J Reardon, Yixuan Ma, Nathaniel S Grabinski, Yalini Ramamoorthy, Rebecca L Packard, Johnathon G Schiebel, Heather L Chandler, Gina M Sizemore

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

8 authors.

Jesse J ReardonThe Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA; Department of Radiation Oncology, The Ohio State University, Columbus, OH, USA.
Yixuan MaDepartment of Radiation Oncology, The Ohio State University, Columbus, OH, USA; Southern Illinois University School of Medicine, Springfield, IL, USA; College of Optometry, The Ohio State University, Columbus, OH, USA.
Nathaniel S GrabinskiThe Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA; Department of Radiation Oncology, The Ohio State University, Columbus, OH, USA.
Yalini RamamoorthyThe Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA; Department of Radiation Oncology, The Ohio State University, Columbus, OH, USA.
Rebecca L PackardThe Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA; Department of Radiation Oncology, The Ohio State University, Columbus, OH, USA.
Johnathon G SchiebelThe Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA; Department of Radiation Oncology, The Ohio State University, Columbus, OH, USA.
Heather L ChandlerCollege of Optometry, The Ohio State University, Columbus, OH, USA. Electronic address: chandler.111@osu.edu.
Gina M SizemoreThe Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA; Department of Radiation Oncology, The Ohio State University, Columbus, OH, USA. Electronic address: gina.sizemore@osumc.edu.

Funding

PDGF-BB and the metastatic brain microenvironmentR37CA282660 · NCI · OHIO STATE UNIVERSITY · PI Gina Marie Sizemore · 2023 to 2026
$1.9M
PDGFR beta signaling in the tumor microenvironment of metastatic breast cancerK22CA218472 · NCI · OHIO STATE UNIVERSITY · PI SIZEMORE, GINA MARIE · 2017 to 2019
$561k
NCI NIH HHS K22 CA218472NCI NIH HHS R37 CA282660
6 · The paper itself

Abstract

introductionCataracts are the world's leading cause of reversible blindness. Although cataract formation is commonly initiated by lens fiber cell defects, cataractogenesis can be characterized by aberrant proliferation and migration of lens epithelial cells. Subsequent overproduction of extracellular matrix components such as fibronectin and collagen by epithelial cells is associated with fibrosis of the lens. Little is known about the role of platelet-derived growth factor receptor β (PDGFRβ) in lens fibrosis. Here, we investigated mice with a conditional knock-in of PDGFRβ hyperactivation using a Fsp1, also known as S100A4, promoter (Fsp1-cre;Pdgfrb

methodsLenses from Fsp1-cre;Pdgfrb

resultsGross examination of cataractous lenses from Fsp1-cre;Pdgfrb

conclusionPDGFRβ promoted cataractogenesis by modulating pro-fibrotic extracellular matrix changes, likely through TGFβ, Wnt/β-catenin, SOCS2, and the STAT5-IGF1 pathways. Future experiments will delineate the precise role of the STAT5-IGF1 signaling pathway in PDGFRβ-mediated fibrosis and the interplay between PDGFRβ and TGFβ in the lens and whether this signaling is targetable to modulate cataractogenesis.

Indexed as

CataractInsulin-Like Growth Factor IReceptor, Platelet-Derived Growth Factor betaTransforming Growth Factor betaAnimalsEpithelial CellsFibrosisLens, CrystallineMiceMice, TransgenicS100 Calcium-Binding Protein A4Signal Transductioninsulin-like growth factor-1, mouseInsulin-Like Growth Factor IReceptor, Platelet-Derived Growth Factor betaS100a4 protein, mouseS100 Calcium-Binding Protein A4Transforming Growth Factor betaCataractIGF1Lens epitheliumPDGFRβSTAT5TGFβ

Identifiers

PMID40953793
PMCPMC13217716

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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.