ArticleThe clinical respiratory journal2025
USP7-Mediated ICAM1 Facilitates Lipopolysaccharide-Induced Human Pulmonary Microvascular Endothelial Cell Injury to Accelerate Pediatric Acute Respiratory Distress Syndrome.
Article in The clinical respiratory journal, 2025. 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIntercellular cell adhesion molecule 1 (ICAM1) has been confirmed to be abnormally expressed in acute respiratory distress syndrome (ARDS) patients. However, its role and mechanism in pediatric ARDS process need further revealed.
methodsSerum samples were selected from pediatric ARDS patients and age-matched healthy individuals. Lipopolysaccharide (LPS)-induced human pulmonary microvascular endothelial cells (HPMECs) were used to mimic ARDS cell models. Cell proliferation and apoptosis were tested by cell counting kit 8 assay, EdU assay, and flow cytometry. Oxidative stress and inflammation were assessed by corresponding kits. M1 macrophage polarization was evaluated via measuring CD86 positive cell rate. The expression levels of ICAM1, ubiquitin-specific peptidase 7 (USP7), and NF-κB pathway-related markers were detected by quantitative real-time PCR and western blot. The interaction between USP7 and ICAM1 was analyzed by Co-IP assay.
resultsLPS induced apoptosis, inflammation, oxidative stress, and M1 macrophage polarization, while suppressed proliferation in HPMECs. ICAM1 was upregulated in pediatric ARDS patients, and its knockdown alleviated HPMEC injury induced by LPS. USP7 positively regulated ICAM1 protein expression through deubiquitination. USP7 overexpression aggravated LPS-induced HPMEC apoptosis, inflammation, oxidative stress, and M1 macrophage polarization. Besides, ICAM1 upregulation could eliminate the inhibitory effect of USP7 knockdown on LPS-induced HPMEC injury. In addition, USP7 activated NF-κB pathway by promoting ICAM1 expression.
conclusionUSP7-mediated ICAM1 upregulation could promote LPS-induced HPMEC injury by activating NF-κB pathway, which provided a new idea for the treatment of pediatric ARDS.
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.