ArticleCell communication and signaling : CCS2025
Soluble E-cadherin contributes to inflammation in acute lung injury via VEGF/VEGFR2 signaling.
Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Proteomic Profile After Intervention With Eplerenone Among Persons With HIV.Open forum infectious diseases · 2026Trial
- Failed Mucosal Allostasis Distinguishes Murine IgG- From IgE-Mediated Recurrent Severe Anaphylaxis.Allergy · 2026Article
- Onion-Mitochondria Inhibit Lipopolysaccharide-Induced Acute Lung Injury by Shaping Lung Macrophage Mitochondrial Function.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- NSC23766 effectively inhibited retinal neovascularization by disrupting the positive feedback loop between Rac1 and VEGFR2.Scientific reports · 2025Article
- Sunitinib treatment reduces proinflammatory cytokine levels and mortality rates by suppressing the NLRP3 inflammasome signaling pathway in sepsis.Inflammopharmacology · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors.
Funding
Abstract
As a gatekeeper of the airway epithelial cells, E-cadherin is not only a critical component for the maintenance of epithelial integrity, but also engaged in pathological processes through the release of a soluble form (sE-cadherin). This study was aimed to investigate the role of sE-cadherin in ALI/ARDS. Serum samples from patients with ARDS and healthy volunteers were collected for the detection of sE-cadherin. An LPS-induced mouse model was induced to analyze the expression of sE-cadherin, and a neutralizing antibody against sE-cadherin (DECMA-1) was given to the LPS-exposed mice. The effects of recombinant sE-cadherin were tested both in vitro and in vivo, and VEGFR2 inhibition was used to explore a possible mechanism for sE-cadherin-induced pulmonary inflammation. We observed an increased level of sE-cadherin in ARDS patients as well as in LPS-exposed mice. In vivo treatment of DECMA-1 significantly attenuated LPS-induced inflammation. In vitro, exogenous sE-cadherin can dramatically upregulate the expression of VEGF in THP1-derived macrophages and human primary macrophages. In addition, intratracheal instillation of recombinant sE-cadherin leads to significant increased infiltration of neutrophils as well as overproduction of IL-6 and IL1β, which could be attenuated by inhibition of VEGF/VEGFR2 signaling. While blockade of the VEGF/VEGFR2 pathway inhibited pulmonary inflammatory responses in LPS-exposed mice. Taken together, our data demonstrated that sE-cadherin contributes to lung inflammation in ALI/ARDS, which is related to activation of the VEGF/VEGFR2 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.