ArticleAdvances in ophthalmology practice and research
Integrated proteomic and metabolomic profiling reveals molecular signatures in cataract patients.
Article in Advances in ophthalmology practice and research. 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: This study aimed to characterize systemic molecular signatures in the serum of patients with age-related cataracts and explore specific variations through integrated proteomic and metabolomic profiling. Methods: Serum samples from 17 cataract patients and 24 healthy controls were analyzed by liquid chromatography-tandem mass spectrometry (LC-MS/MS) for proteomic and metabolomic profiling. Differentially expressed proteins (DEPs) and metabolites (DEMs) were identified using multivariate statistics. Functional enrichment and multi-omics integration analyses were performed to identify key biological pathways. Key proteins were validated via enzyme-linked immunosorbent assay (ELISA) in an independent cohort (n=136). Results: We identified 257 DEPs and 51 significant DEMs in cataract patients. Downregulated proteins included peroxiredoxin 6 (PRDX6), biliverdin reductase B (BLVRB), glycolytic enzyme phosphoglycerate kinase 1 (PGK1), and chaperone peptidylprolyl isomerase A (PPIA), while oxidative stress-related metabolites were elevated. Age-stratified analysis showed distinct profiles in younger patients (45-55 years). Multi-omics integration demonstrated strong correlation between proteome and metabolome, with co-enrichment in pathways such as prolactin signaling and diabetic cardiomyopathy. ELISA validation confirmed decreased levels of PGK1 and PPIA in an independent cohort. Conclusions: Our findings reveal systemic molecular alterations in age-related cataracts, highlighting oxidative stress and metabolic dysregulation with age-specific patterns. These results provide insights into cataract pathogenesis and potential biomarkers for personalized risk assessment.
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.