ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2026
Role of Autophagy in Scleral Remodeling During Form-Deprivation Myopia.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 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
3 authors.
Funding
Abstract
Autophagy has been implicated in tissue remodeling, but its role in scleral remodeling during myopia development and in atropine-mediated myopia control remains unclear. We investigated this issue using complementary in vitro and in vivo models. Human scleral fibroblasts (HSFs) were exposed to hypoxia and treated with rapamycin (RAPA) or 3-methyladenine (3-MA). Beclin-1 knockdown and bafilomycin A1 (BafA1)-based LC3B II accumulation assays were used to assess the functional contribution of autophagy and autophagic flux. In vivo, form-deprivation myopia (FDM) was induced in guinea pigs, followed by atropine, RAPA, or 3-MA intervention. Refractive error, axial length, scleral histology, extracellular matrix remodeling, autophagy-related markers, and AMPK/mTOR/P70S6K signaling were evaluated. Hypoxia induced a remodeling phenotype in HSFs, characterized by decreased COL1A1 and increased MMP2/α-SMA, accompanied by increased autophagy. 3-MA attenuated these changes, whereas RAPA aggravated them. Beclin-1 knockdown similarly suppressed hypoxia and RAPA-associated remodeling changes and reduced autophagic flux, supporting a functional role of autophagy in hypoxia-induced scleral fibroblast remodeling. In FDM guinea pigs, scleral tissue showed increased HIF-1α expression, autophagy activation, and extracellular matrix remodeling. Both 0.05% and 1% atropine slowed myopia progression and axial elongation, improved scleral structural abnormalities, and suppressed autophagy-related changes, with no significant difference between the two concentrations. Subconjunctival RAPA exacerbated, whereas 3-MA alleviated, myopia progression and scleral remodeling. These findings suggest that excessive scleral autophagy links hypoxic stress to scleral extracellular matrix remodeling in experimental myopia. This process may also contribute to the anti-myopic action of atropine.
Indexed as
Identifiers
What Socratic 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 Socratic graph.