Background: Acute respiratory distress syndrome (ARDS) is characterized by non-cardiogenic pulmonary edema caused by inflammation, which can lead to serious respiratory complications. Due to the high mortality of ARDS caused by sepsis, biological markers that enable early diagnosis are urgently needed for clinical treatment.
Methods: In the present study, we used the public microarray data of whole blood from patients with sepsis-induced ARDS, patients with sepsis-alone and healthy controls to perform an integrated analysis based on differential expressed genes (DEGs) and co-expression network to identify the key genes and pathways related to the development of sepsis into ARDS that may be key targets for diagnosis and treatment.
Results: Compared with controls, we identified 180 DEGs in the sepsis-alone group and 152 DEGs in the sepsis-induced ARDS group. About 70% of these genes were unique to the two groups. Functional analysis of DEGs showed that neutrophil-mediated inflammation and mitochondrial dysfunction are the main features of ARDS induced by sepsis. Gene network analysis identified key modules and screened out key regulatory genes related to ARDS. The key genes and their upstream regulators comprised a gene panel, including EOMES, LTF, CSF1R, HLA-DRA, IRF8 and MPEG1. Compared with the healthy controls, the panel had an area under the curve (AUC) of 0.900 and 0.914 for sepsis-alone group and sepsis-induced ARDS group, respectively. The AUC was 0.746 between the sepsis-alone group and sepsis-induced ARDS group. Moreover, the panel of another independent blood transcriptional expression profile dataset showed the AUC was 0.769 in diagnosing sepsis-alone group and sepsis-induced ARDS group.
Conclusions: Taken together, our method contributes to the diagnosis of sepsis and sepsis-induced ARDS. The biological pathway involved in this gene biomarker panel may also be a critical target in combating ARDS caused by sepsis.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10339646 | PMC |
| http://dx.doi.org/10.1186/s12920-023-01595-8 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
H3K14la drives endothelial dysfunction in sepsis-induced ARDS by promoting SLC40A1/transferrin-mediated ferroptosis.
MedComm (2020)
February 2025
Pulmonary endothelial cell (EC) activation is a key factor in acute respiratory distress syndrome (ARDS). In sepsis, increased glycolysis leads to lactate buildup, which induces lysine lactylation (Kla) on histones and other proteins. However, the role of protein lactylation in EC dysfunction during sepsis-induced ARDS remains unclear.
View Article and Find Full Text PDFCromolyn sodium reduces LPS-induced pulmonary fibrosis by inhibiting the EMT process enhanced by MC-derived IL-13.
Respir Res
January 2025
Department of Anesthesiology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, 210011, Jiangsu Province, China.
Background: Sepsis is a systemic inflammatory response caused by infection. When this inflammatory response spreads to the lungs, it can lead to acute lung injury (ALI) or more severe acute respiratory distress syndrome (ARDS). Pulmonary fibrosis is a potential complication of these conditions, and the early occurrence of pulmonary fibrosis is associated with a higher mortality rate.
View Article and Find Full Text PDFLIN28A-dependent lncRNA NEAT1 aggravates sepsis-induced acute respiratory distress syndrome through destabilizing ACE2 mRNA by RNA methylation.
J Transl Med
January 2025
Emergency Department, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510630, China.
Background: Acute respiratory distress syndrome (ARDS) is a life-threatening and heterogeneous disorder leading to lung injury. To date, effective therapies for ARDS remain limited. Sepsis is a frequent inducer of ARDS.
View Article and Find Full Text PDFStudy on the Mechanism of UMI-77 in the Treatment of Sepsis-Induced Acute Lung Injury Based on Transcriptomics and Metabolomics.
J Inflamm Res
December 2024
Department of Critical Care Medicine, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, Taizhou, 317000, People's Republic of China.
Introduction: Sepsis-induced acute lung injury (ALI), a critical sequela of systemic inflammation, often progresses to acute respiratory distress syndrome, conferring high mortality. Although UMI-77 has demonstrated efficacy in mitigating lung injury in sepsis, the molecular mechanisms underlying its action have not yet been fully elucidated.
Methods: This study aimed to delineate the mechanism by which UMI-77 counteracts sepsis-induced ALI using comprehensive transcriptomic and metabolomic analyses.
Verapamil inhibits ferroptosis in septic acute lung injury by blocking L-type calcium channels.
Biochem Biophys Res Commun
January 2025
Immunology Department of Hebei Medical University, Shijiazhuang, PR China. Electronic address:
Acute lung injury (ALI) and its severe form, acute respiratory distress syndrome (ARDS), result from pulmonary edema and alveolar-capillary barrier disruption due to inflammation, often triggered by conditions like sepsis. Sepsis-induced ALI (SALI) involves extensive damage to vascular endothelium and alveolar epithelium, leading to respiratory failure. Our study explores ferroptosis, an iron-dependent cell death pathway, and calcium dysregulation in SALI.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!