The IGF2-ERK-Fos axis drives a Müller cell glial-mesenchymal transition-like response to disrupt retinal…

Animal / preclinicalCell communication and signaling : CCS· Jul 2026

The IGF2-ERK-Fos axis drives a Müller cell glial-mesenchymal transition-like response to disrupt retinal homeostasis in early myopia.

Jiaojiao Feng, Xiaoqi Gong, Yibo Han … Hongsheng Bi

RetinaAnimal / preclinicalQ1IF 11.2

Retinal support cells expand sharply in early experimental myopia.

The IGF2-ERK-Fos axis drives a Müller cell glial-mesenchymal transition-like response to disrupt retinal homeostasis in early myopia.

Jiaojiao Feng … Hongsheng Bi

Cell communication and signaling · Jul 2026

Background

Myopia is increasingly recognized as a complex pathology involving retinal remodeling, yet the cellular mechanisms linking early visual stress to this process remain unclear.

Purpose

This study investigated whether Müller glial (MG) cells undergo a glial-mesenchymal transition (glial-mesenchymal transition)-like response in early myopia and identified the upstream signaling axis driving this transformation.

18.9%

Results

18.9%

vs. 6.9%

Müller support cells made up nearly 3× more of retinal cells

More results

IGF2 signaling was elevated in myopic MG cells and correlated with ERK/Fos activation.

More results

In vivo siIGF2 attenuated myopia progression, preserved retinal function/structure, suppressed MG activation/proliferation and glial-mesenchymal transition/extracellular matrix marker expression, and reduced inner limiting membrane abnormalities and retinal stiffening.

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Conclusion

The IGF2-ERK-Fos axis is a key upstream driver of this pathology, presenting a novel target for intervention to preserve retinal homeostasis.

The IGF2-ERK-Fos axis drives a Müller cell glial-mesenchymal transition-like response to disrupt retinal homeostasis in early myopia.

The IGF2-ERK-Fos axis drives a Müller cell glial-mesenchymal transition-like response to disrupt retinal homeostasis in early myopia.

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