IGF2BP3 promotes diabetic retinopathy development by enhancing SEMA3G mRNA stability

Graphical abstract

IGF2BP3 promotes diabetic retinopathy development by enhancing SEMA3G mRNA stability
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Keywords

Angiogenesis
Cell proliferation
Cytokines
Diabetic retinopathy
Gene regulation
IGF2BP3
Inflammation
Microvascular proliferation
mRNA stability
Retinal pathology
SEMA3G

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How to Cite

1.
Chen Y, Zhao T, Han M, Chen Y. IGF2BP3 promotes diabetic retinopathy development by enhancing SEMA3G mRNA stability. Electron. J. Biotechnol. [Internet]. 2026 Sep. 15 [cited 2026 Sep. 17];83:100723. Available from: https://www.ejbiotechnology.info/index.php/ejbiotechnology/article/view/2591

Abstract

Background: Diabetic retinopathy is characterized by excessive microvascular proliferation that leads to vitreous hemorrhage, retinal traction, and subsequent visual impairment. Aberrant expression of IGF2BP3 is involved in the pathogenesis of multiple diseases. This study aimed to elucidate the mechanism by which IGF2BP3 mediates diabetic retinopathy by regulating semaphorin-3G (SEMA3G) expression.

Results: Elevated IGF2BP3 expression was observed in diabetic retinopathy. In vitro, IGF2BP3 overexpression promoted pathological angiogenesis, whereas its knockdown significantly attenuated wound healing, reduced inflammatory cytokine secretion, and suppressed cellular proliferation. A targeted regulatory relationship between IGF2BP3 and SEMA3G mRNA was identified, with IGF2BP3 enhancing SEMA3G mRNA stability. SEMA3G was upregulated in diabetic retinopathy, and its overexpression partially rescued the diabetic retinopathy progression suppressed by IGF2BP3 silencing. In vivo, IGF2BP3 overexpression aggravated histopathological alterations, thereby accelerating diabetic retinopathy development.

Conclusions: In summary, IGF2BP3 promotes diabetic retinopathy development by enhancing SEMA3G mRNA stability.

https://doi.org/10.1016/j.ejbt.2026.100723
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References

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