ArticleScientific reports2026
Persistent loss of membrane-associated MUC4 reprograms physiological functions in corneal epithelial cells via MAPK-dependent cascade.
Article in Scientific reports, 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
Mucin-4 (MUC4), a key membrane-associated mucin of the corneal apical glycocalyx, plays an important role in maintaining corneal epithelial homeostasis and wettability. Dysregulation of MUC4 has been associated with barrier dysfunction and ocular surface inflammation. This study aimed to investigate the physiological regulatory role of MUC4 in human corneal epithelial cells (HCEs) and elucidate its underlying intracellular mechanisms. MUC4 in HCEs was silenced through lentivirus-based shMUC4 pseudovirion transduction. Cell viability was analyzed via CCK-8 reagent. Cell motility was monitored via real-time culture monitoring system. Mitochondrial function was analyzed by Seahorse analyzer. Expressions of associated proteins were determined by immunoblotting. Changes in phosphorylation levels in major signaling pathways were determined by protein arrays. MUC4 increased time-dependently in HCEs. The expression was efficiently silenced by shMUC4 transduction. MUC4 loss suppressed cell viability through increasing caspase-8 and PARP1 as well as decreasing Bcl-2 and Bcl-xL. MUC4 loss promoted cell motility by increasing the phosphorylation of FAK-Y397 and paxillin-Y118. Maximal respiration and spare respiratory capacity were lower in MUC4-silenced HCEs by decreasing expression of key mitochondrial proteins (ATP8, MT-ND1, MT-ND3, MT-ND5, MT-CO2, and MT-CO3). MUC4 loss activated FAK and triggered the activation of MAPK-associated kinases in HCEs. These findings indicated that persistent MUC4 production maintained cell viability and hindered migration in corneal epithelial cells via FAK/MAPK/P38 signaling pathway.
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.