Calcitriol attenuates form-deprivation myopia through VDR-mediated inhibition of NF-κB signaling and scleral remodeling.

Authors

Rongbin Liang, Meilin Li, Jiakun Li, Yulu Zhou, Tao Li, Xiangjia Zhu, Xiaodong Zhou

Published in

International immunopharmacology. Volume 188. Pages 117376. Sep 06, 2026. Epub Sep 06, 2026.

Abstract

To investigate the role and mechanisms of calcitriol in form-deprivation myopia (FDM).
Calcitriol was evaluated in a guinea pig FDM model and a tumor necrosis factor-alpha (TNF-α)-induced inflammatory model using human retinal pigment epithelial (RPE) cells. Vitamin D receptor (VDR) dependence was assessed by adeno-associated virus- or small interfering RNA-mediated VDR knockdown. Refractive status, axial length, fundus changes, scleral collagen remodeling, inflammatory cytokines, nuclear factor kappa-B (NF-κB) activation, and matrix metalloproteinase-2 (MMP2) expression were examined. Protein interaction analysis explored VDR-NF-κB p65 interaction.
Calcitriol significantly attenuated FDM progression in guinea pigs, reducing myopic refractive shift, axial elongation, and fundus alterations. It increased scleral collagen expression and improved collagen organization and ultrastructure. Calcitriol also decreased circulating and retinal TNF-α, interleukin-1β, and interleukin-6 levels, accompanied by NF-κB inhibition and MMP2 downregulation. VDR knockdown markedly weakened the protective effects of calcitriol on refractive and axial changes, inflammatory cytokine production, and NF-κB/MMP2 signaling. In vitro, calcitriol inhibited TNF-α-induced NF-κB p65 nuclear translocation and reduced inflammatory cytokine secretion and MMP2 expression in RPE cells; these effects were largely abolished by VDR knockdown. Protein interaction analysis suggested that calcitriol enhanced VDR-NF-κB p65 interaction, thereby restricting NF-κB activation.
Calcitriol delays FDM progression through VDR-mediated inhibition of NF-κB activation, reducing inflammatory cytokine production, MMP2 expression, scleral collagen degradation, and tissue remodeling.

PMID:
42702162
Bibliographic data and abstract were imported from PubMed on 07 Sep 2026.

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