ArticleUpsala journal of medical sciences2026
Endocan attenuates LPS-induced alveolar type II cells injury through PI3K/Akt/mTOR pathway.
Article in Upsala journal of medical sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- ATPR promotes differentiation in gastric cancer cells by endocan.Molecular biology reports · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Alveolar type II (AT2) cell injury plays an important role in the pathogenesis of acute lung injury (ALI), but the corresponding treatment options are limited in clinical practice. Endocan has been proved to exert a protective effect in ALI, however, the underlying mechanism remains unclear. The phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mechanistic target of rapamycin (mTOR) signaling pathway was found to exhibit beneficial effects in lipopolysaccharide-induced ALI. This study aimed to investigate protective effects of endocan on AT2 cells and the signal pathway in LPS-induced ALI. Methods: Pulmonary function testing and hematoxylin-eosin staining were employed to evaluate the effects of endocan on the LPS-induced ALI in mice. Transmission electron microscopy (TEM) analysis, immunofluorescence and Western blot were used to assess the AT2 protection of endocan. Mouse lung epithelial cell line 12 (MLE-12) cells were facilitated to observe the activation of PI3K/AKT/mTOR pathway. Results: Endocan administration effectively ameliorated respiratory parameters in LPS-challenged ALI mice. TEM revealed that endocan treatment preserved AT2 cell integrity and maintained lamellar body ultrastructure compared to the mice injected LPS only. Western blot analysis showed a higher surfactant protein C expression in endocan-treated mice than that of model group. Moreover, the phosph-PI3K, -AKT, -mTOR levels detected by Western blot were significantly observed upregulated after endocan treatment. However, rapamycin, an mTOR inhibitor, abolished the protective effects of endocan against ALI, indicating this pathway may be critical for its action on AT2 cells. In LPS-treated MLE-12 cells, the Western blot analysis further confirmed that rapamycin suppressed endocan-induced activation of the PI3K/AKT/mTOR pathway, thereby attenuating the protective effects of endocan on MLE-12 cells. Conclusion: Endocan protects AT2 cells against ALI through activating PI3K/AKT/mTOR pathway, suggesting its therapeutic potential for AT2 in patients with ALI.
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.