ReviewExperimental eye research2025
Investigating prolactin-induced protein and its role in modulating the metabolic state of the keratoconus microenvironment.
Review in Experimental eye research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- Update on the Physiopathology of Keratoconus.Medical sciences (Basel, Switzerland) · 2026Review
- Sex Hormones and Keratoconus: In Search of the Link.Journal of clinical medicine · 2026Article
- Optimization and Application of Seahorse Glycolytic Stress Test in Mouse Corneal Tissues: Revealing Metabolic Profiles in Injury Models.Investigative ophthalmology & visual science · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Keratoconus (KC) is a progressive corneal disorder characterized by thinning and irregular astigmatism, leading to visual impairment. This study investigates the role of Prolactin-Induced Protein (PIP), a 17-kDa glycoprotein significantly downregulated in KC subjects, in modulating corneal cellular metabolism. Using human corneal fibroblasts from healthy (HCFs) and KC (HKCs) subjects, we assessed the effects of exogenous PIP (50-500 ng/mL) via targeted mass spectrometry and Seahorse bioenergetic analyses. Metabolomic profiling revealed that PIP significantly modulates various metabolites involved in multiple bioenergetic and oxidative stress related pathways including the Warburg effect and thiamine metabolism. Seahorse analysis revealed that when compared to HCFs, HKCs exhibit impaired ATP production from both oxidative phosphorylation and glycolysis. Notably, PIP treatment reversed this impairment and selectively enhanced mitochondrial function and glycolysis in HKCs without affecting HCFs. This study provides the first evidence of PIP's role in regulating energy metabolism in KC, suggesting its potential as a therapeutic target for addressing the metabolic dysfunction underlying KC pathogenesis.
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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.