ArticleJournal of inflammation research2021
OLFM4 Regulates Lung Epithelial Cell Function in Sepsis-Associated ARDS/ALI via LDHA-Mediated NF-κB Signaling.
Article in Journal of inflammation research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 58 citations in OpenAlex.
- The multidimensional signaling of ELANE: from congenital hematopoietic failure to immune microenvironment crosstalk and targeted interventions.Cell communication and signaling : CCS · 2026Review
- S100A9 lactylation facilitated sepsis-related acute respiratory distress syndrome via promoting transcription activation of IL-1β in macrophages.Cell communication and signaling : CCS · 2026Article
- Loss of MLKL impairs abdominal aortic aneurysm development by attenuating smooth muscle cell necroptosis.Cell death & disease · 2026Article
- YBX1 orchestrates LDHA-mediated metabolic reprogramming and NF-κB activation to drive clear cell renal cell carcinoma progression.Cell death & disease · 2026Article
- OLFML3 negatively regulates RIG-I signaling in RNA virus infection.Frontiers in immunology · 2026Article
- Olfactomedin-4 elevation in pediatric acute respiratory distress syndrome.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Advances in acute respiratory distress syndrome: focusing on heterogeneity, pathophysiology, and therapeutic strategies.Signal transduction and targeted therapy · 2025Review
- Plasma-derived extracellular vesicles prime alveolar macrophages for autophagy and ferroptosis in sepsis-induced acute lung injury.Molecular medicine (Cambridge, Mass.) · 2025Article
- H3K14la drives endothelial dysfunction in sepsis-induced ARDS by promoting SLC40A1/transferrin-mediated ferroptosis.MedComm · 2025Article
- A potential XGBoost Diagnostic Score forFrontiers in immunology · 2025Article
- From "metabolic storm" to "immune paralysis": the dynamic evolution of macrophages and metabolism reprogramming in ARDS.Frontiers in immunology · 2025Review
- Unlocking the secrets of glucose metabolism reprogramming: the role in pulmonary diseases.Frontiers in pharmacology · 2025Review
- Polymethoxyflavones extracted fromFrontiers in pharmacology · 2025Article
- Nogo-A exacerbates sepsis-associated encephalopathy by modulating microglial SHP-2/NLRP3 balance and inducing ROS and M1 polarization.Biomolecules & biomedicine · 2024Article
- Gene Expression Dysregulation in Whole Blood of Patients withInternational journal of molecular sciences · 2024Article
- Construction of a NETosis-related gene signature for predicting the prognostic status of sepsis patients.Heliyon · 2024Article
- Bibliometric study of sepsis-associated liver injury from 2000 to 2023.World journal of gastroenterology · 2024Article
- Article
- Fibroblast Growth Factor 21 Relieves Lipopolysaccharide-Induced Acute Lung Injury by Suppressing JAK2/STAT3 Signaling Pathway.Inflammation · 2024Article
- Characterization of 3,3'-iminodipropionitrile (IDPN) damaged utricle transcriptome in the adult mouse utricle.Frontiers in molecular neuroscience · 2024Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute respiratory distress syndrome (ARDS) is one of the leading causes of death in patients with sepsis. As such, early and accurate identification of sepsis-related ARDS is critical.
methodsBioinformatic analysis was used to explore the GEO datasets. ELISA method was used to detect the plasma or cellular supernatant of relevant proteins. Quantitative real-time PCR was used for mRNA measurements and Western blot was applied for protein measurements. Immunohistochemistry staining and Immunofluorescence staining were used to identify the localization of OLFM4. Cecal ligation and puncture (CLP) model was used to establish sepsis model.
resultsThe bioinformatic analysis results identified ten genes (
conclusionOLFM4 may regulate the pro-inflammatory response of lung epithelial cells in sepsis-related ARDS by modulating metabolic disorders; this result could provide new insights into the treatment of sepsis-induced ARDS.
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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.