ArticleRespiratory research2026
ROMO1 is involved in airway mucus hypersecretion in COPD through the mitochondrial ROS-STAT6 pathway.
Article in Respiratory research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Integrative multi-omics reveals NQO1-mediated airway epithelial injury as a key mechanism of bisphenol A-induced COPD.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Mitochondrial dysfunction and the regulatory cell death crosstalk network in chronic obstructive pulmonary disease: from oxidative stress mechanisms to targeted therapeutic strategies.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
backgroundOxidative stress contributes to airway mucus hypersecretion in the pathogenesis of chronic obstructive pulmonary disease (COPD). Although reactive oxygen species modulator 1 (ROMO1) is involved in mitochondrial oxidative stress, its role in airway mucus hypersecretion in COPD remains unclear.
methodsThe protein expression of ROMO1 and mucin5AC (MUC5AC) in human airway epithelium was determined by immunohistochemistry. The effects of ROMO1 on mitochondrial injury and MUC5AC expression in cigarette smoke extract (CSE)-treated airway epithelial cells were evaluated by a series of experimental techniques, including real-time PCR, western-blot and immunofluorescent staining.
resultsProtein expression of ROMO1 and MUC5AC was significantly elevated in the airway epithelium of COPD patients compared with the controls. The mRNA and protein expression of ROMO1 and MUC5AC were significantly increased in concentration- and time-dependent manners when airway epithelial cells were treated with CSE. ROMO1 silencing significantly suppressed 7.5% CSE-induced mitochondrial structure damage, mitochondrial membrane potential loss, intracellular ATP depletion, mitochondrial reactive oxygen species production, signal transducer and activator of transcription 6 (STAT6) phosphorylation, and MUC5AC expression in airway epithelial cells. Moreover, pretreatment with either a mitochondrial-targeted antioxidant or STAT6 inhibitor significantly inhibited the up-regulated expression of p-STAT6/STAT6 and MUC5AC in airway epithelial cells stimulated with 7.5% CSE.
conclusionOur findings suggest that ROMO1 contributes to airway mucus hypersecretion in COPD by mediating MUC5AC expression in airway epithelial cells via the mitochondrial ROS-STAT6 pathway, thereby highlighting its potential clinical value as a therapeutic target.
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.