ArticleApplied biochemistry and biotechnology2025
Inhibition of the Foxo3/Txnip Axis Alleviates Ventilator-Induced Diaphragmatic Dysfunction by Downregulating MuRF1.
Article in Applied biochemistry and biotechnology, 2025. 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
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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.
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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.
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Who cites it
2 citing papers in PubMed.
- VIDD or CIADD? The ventilator remains a bona fide culprit.BMC anesthesiology · 2026Article
- The Role of TXNIP in Skeletal Muscle Physiology and Related Diseases: Current Perspectives.Journal of inflammation research · 2026Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Ventilator-induced diaphragm dysfunction (VIDD) is one of the main causes of weaning from mechanical ventilation (MV). The forkhead box O3 (Foxo3) has been identified as being involved in regulating the contractile function of skeletal muscle. This study aimed to figure out the regulatory role and mechanism of Foxo3 on VIDD. The mouse myoblast C2C12 cells were stimulated using different intensities of stress to mimic the in-vitro VIDD model. 3- (4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and TdT-mediated dUTP nick end labeling (TUNEL) assays were applied to check cell viability and apoptosis, respectively. Cellular inflammation and oxidative stress levels were evaluated by measuring cellular inflammatory factors (IL-1β and TNF-α) and oxidative stress markers (SOD and MDA). The release of oxygen species (ROS) was assayed by cellular immunofluorescence. The expression of apoptosis-associated proteins (Bax and Bcl-2), Gpx4, Slc7a11, Ptgs2, Foxo3, Txnip, Murf1, Atrogin-1, Nlrp3, Asc, and Caspase1 was gauged using Western blot. The rats with or without MV therapy were treated with the Foxo3 inhibitor Carbenoxolone (CBX) to characterize the impact of Foxo3 on VIDD. Stress stimulation dampened myogenic cell viability, boosted apoptosis, inflammation, oxidative stress, and ROS release, and activated the expression of Foxo3 and Txnip pathways. Overexpression of Txnip or Murf1 lessened the protective effect of FOxO3 inhibition on myoblasts. Downregulation of Txnip or Murf1 mitigated myoblasts dysfunction that was induced by Foxo3 overexpression. In vivo, inhibition of Foxo3 mitigated MV-induced diaphragmatic atrophy and reduced contractility, inflammation, and oxidative stress in rats. Inhibition of Foxo3 eased VIDD by downregulating Txnip and Murf1.
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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.