ArticleJournal of translational medicine2025
Bone morphogenetic protein 10 serves as a biomarker and a potential therapeutic target for endothelial dysfunction in endotoxin-induced acute lung injury.
Article in Journal of translational medicine, 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
7 authors.
Funding
Abstract
backgroundEndothelial dysfunction plays a crucial role in the development of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) in critically ill patients. Bone Morphogenetic Protein 10 (BMP10) has been demonstrated to promote cardiovascular development and cell proliferation, support endothelial quiescence, and inhibit endothelial apoptosis. Furthermore, BMP10 has been identified as a novel biomarker for predicting the severity and clinical outcomes of various disorders. However, its role in modulating endotoxin-induced ALI remains unclear.
methodsC57BL/6 mice were administered lipopolysaccharide (LPS) via intratracheal instillation to induce ALI, followed by intraperitoneal injection of BMP10 as a treatment. Simultaneously, primary human pulmonary microvascular endothelial cells (HPMECs) were used to model LPS-induced endothelial dysfunction in vitro. Additionally, plasma BMP10 levels in critically ill patients with pneumonia-related acute respiratory failure (ARF) were measured using EKISA kits.
resultsHematoxylin and eosin staining of murine lung sections showed that BMP10 treatment mitigated LPS-induced alveolar interstitial thickening, edema, and inflammatory cell infiltration. Immunohistochemistry, immunofluorescence (IF) staining, and Western blot analysis of murine lung tissues revealed LPS stimulation reduced the expression of VE-cadherin and the anti-apoptotic protein MCL-1. Additionally, LPS stimulation increased the levels of ICAM-1, VCAM-1, and angiopoietin-2, highlighting evidence of endothelial dysfunction. BMP10 treatment reversed these effects. IF staining and Western blot analysis of HPMECs revealed a decrease in VE-cadherin expression and an increase in ICAM-1 and VCAM-1 following LPS stimulation. These changes were reversed by BMP10 pretreatment. Moreover, Western blot analysis of murine lung homogenates and HPMECs showed that LPS stimulation decreased the expression of pSmad1/5/8, a marker of BMP10-associated canonical signaling pathway, but BMP10 treatment restored their activation. Plasma BMP10 levels measured on the day of recruitment and 2 days later were significantly higher in critically ill patients with pneumonia-related ARF who died in the hospital compared to those who survived.
conclusionsBMP10 improved LPS-induced ALI by mitigating endothelial dysfunction. Additionally, plasma BMP10 serves as a biomarker for predicting mortality in critically ill patients with pneumonia-related ARF. These findings highlight the important role of BMP10 in developing new therapeutic strategies for treating ALI and 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.