ArticleRespiratory research2026
Exosomes derived from bone marrow mesenchymal stem cells alleviate sepsis-induced ARDS via inhibition of HOXA9-mediated glycolysis in alveolar macrophages.
Article in Respiratory research, 2026. 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
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
2 citing papers in PubMed.
- MSCs and MSC-Exos in pediatric ARDS treatment: translational research and the reshaping of nursing roles.Frontiers in pediatrics · 2026Review
- Mitochondrial dysfunction in ARDS: unraveling the regulatory networks and therapeutic opportunities.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
backgroundPulmonary injury in sepsis often develops into acute respiratory distress syndrome (ARDS), in which the polarization state of alveolar macrophages (AMs) is a central pathogenic factor. Bone marrow mesenchymal stem cell-derived exosomes (BMSCs-exo) have demonstrated therapeutic potential in septic ARDS through metabolic modulation, yet the specific mechanisms remain unclear. This study investigated whether BMSCs-exo attenuate ARDS by regulating AM polarization via glycolysis inhibition and clarified the role of HOXA9.
methodsBMSCs were identified using flow cytometry and trilineage differentiation. BMSCs-exo were characterized by transmission electron microscopy, nanoparticle tracking analysis and Western blot. An in vitro septic model was established by stimulating MH-S cells with lipopolysaccharide (LPS, 1 µg/mL). In vivo, ARDS was induced in C57BL/6 mice using either LPS (10 mg/kg) or cecal ligation and puncture (CLP), followed by caudal vein injection of BMSCs-exo. Glycolysis and macrophage polarization were evaluated with Western blot, RT-qPCR, and immunofluorescence.
resultsBMSCs-exo treatment improved survival in septic mice, alleviated pulmonary inflammation and edema, suppressed glycolysis in AMs, and restored M1/M2 balance. In vitro, BMSCs-exo downregulated glycolysis-associated markers in LPS-stimulated MH-S cells, suppressed M1 polarization, and facilitated M2 polarization. Notably, knockdown of the HOXA9 gene significantly diminished the ability of BMSCs-exo to suppress glycolysis and M1 polarization in MH-S cells.
conclusionBMSCs-exo mitigate sepsis-induced ARDS by inhibiting HOXA9-mediated glycolysis and re-establishing AM polarization homeostasis, supporting their potential as a promising therapeutic approach for 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.