ArticleResearch in pharmaceutical sciences2026
GPR97 variants and their influence on pathological myopia: implications for glucocorticoid treatment.
Article in Research in pharmaceutical 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.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background and purpose: Pathologic myopia (PM) is a severe form of myopia associated with structural changes in the eye, leading to vision impairment. Identifying genetic factors that contribute to PM can enhance the treatment of the condition. This study aimed to investigate the association between the Experimental approach: A cohort of 412 sporadic PM patients underwent Sanger sequencing and genotyping for GPR97 gene variants. Thirty-one PM patients with various GPR97 genotypes received glucocorticoid and brinzolamide treatment over 24 months. Real-time PCR was employed to examine the target gene mRNA expression. A scratch assay was performed to detect cell migration ability. Findings/Results: A significant association was identified between GPR97 rs76688596 genotypes and PM occurrence. The CC genotype was linked to elevated intraocular pressure (IOP). In human scleral fibroblasts, overexpression of GPR97 Arg396 resulted in upregulation of IOP-related genes serine/arginine-rich splicing factor 3, peptidyl-prolyl cis-trans isomerase 4, peptidyl-prolyl cis-trans isomerase 5, and nuclear receptor subfamily 3 group C member 1. The GPR97 Arg396 mutation inhibited the glucocorticoid-GPR97 axis and reduced cell migration ability. Clinically, CC genotype carriers exhibited significant improvements in axial length, spherical equivalent, IOP, best-corrected visual acuity, and visual field mean sensitivity with glucocorticoid treatment. Conclusion and implications: The study revealed that the GPR97 rs76688596 G > C variant is associated with PM pathogenesis, influencing gene expression related to IOP. The differential response to glucocorticoid treatment among GPR97 genotypes suggests personalized therapeutic potential.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.